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Fifteenth International Congress on 
Hygiene and Demography 


September 23-28, 1912 




Hygienic Microbiology and Parasitology 







* *i 


> OF T©* 




Prof. Theobald Smith. M. D., Harvard Medical School, Boston. 


Prof. Friedrich Loeefler, Greifswald, Germany. 
Prof. August Gaertner, Jena, Germany. 
Prof. George H. F. Nuttall, Cambridge, England. 
Prof. Adolf Dieudonne, Munich, Germany. 
Prof. Alfred Pettersson, Stockholm, Sweden. 
Regierungsrat Dr. A. Weber, Berlin, Germany. 
Prof. Karl Landsteiner, Vienna, Austria. 


Prof. Wm. H. Park, M. D., Research Laboratory. Department of 

Health, New York City. 
Prof. Charles Wardell Stiles, Ph. D., United States Public Health 

Service, Washington. D. C. 


Prof. Hibbert W. Hill, M. D., University of Minnesota, Minneapolis. 
Prof. Philip Hanson Hiss, Jr., M. D., 1 Medical Department, Colum- 
bia University, New York City. 

1 Prof . Philip Hanson Hiss, professor of bacteriology in the College of Physi- 
cians and Surgeons, New York, died February 27, 1913, in the forty-sixth year 
of his age. 



Report of the Secretary 3 

Some Experiments upon the Nature of the Virus of Rabies 9 

Drs. D. W. Poor and Edna Stein hardt. 

Natural and Induced Immunity to Typhus Fever 17 

Drs. John F. Anderson and Joseph Goldberger. 

Observations on a Chicken Sarcoma and its Filterable Cause 26 

Drs. Peyton Rous and John B. Murphy. 

Ueber Choleraelektivnahrboden 33 

Prof. Adolf Dieudonne. 

Egg-agar as Culture Medium for Cholera Spirilla 39 

Dr. Charles Krumwiede, Jr. 

The use of Calcium Carbonate in Solid Media for the Differentiation of 

Sugar-fermenting Bacteria, especially of the Colon-typhoid Group 40 

Dr. A. J. Bendick. 

Special Culture Media for Pure Culture of Amebae found in the Intestines 

of Animals 43 

Dr. Anna W. Williams. 

The Bacterial Examination of Water 47 

Prof. E. O. Jordan. 

Cultivation of Malarial Plasmodia in Vitro 51 

Dr. C. C. Bass. 

A Critical Review of the Bacteriology of Human Leprosy (with special 

Reference to the Chromogenic and Nonchromogenic Acid-fast Strains) _ 52 

Dr. Charles W. Duval. 

Influenzal Meningitis; Experimental and Clinical 57 

Dr. Martha Wollstein. 

Protective Inoculation. Experimental and Clinical Studies on the Use of 
Leucocyte Extract in the Treatment of Erysipelas, Pneumonia, and 
other Infections 62 

Dr. P. Hanson Hiss. 

The Production of Antirabic Immunity by Intraspinal Injections of 

Virus 1 75 

Dr. D. L. Harris. 

The Etiology of Trachoma 79 

Dr. Anna W. Williams. 



Paratyphus und paratyphus-ahnliche Bakterien mit besonderer Bertick- 
sichtigung ihrer Yerbreitung in der Aussenwelt und ihrer Beziehun- 

gen zu Mensch und Tier 83 

Gen. Reg. Rat, Dr. A. Weber. 

On the Organisms of the Typhoid-Colon Group and their Differentiation. 99 

Dr. J. Henderson Smith. 

Sur les Salmonelloses (bacilles paratyphiques B, bacilles des empoisson- 

nements alimentaires, etc.) 118 

Prof. Dr. Sacqtjepee. 

Representatives of the Gaertner Group Isolated from the Tissues of 

Laboratory Animals 127 

Dr. John C. Torrey. 

Bacteriological Examination of Market Milk 133 

Dr. P. G. Heinemann. 

La Tuberculosis Experimental en las Grandes Alturas 139 

Dr. Nestor Morales. 

Milzbrand und Salvarsan 146 

Dr. Georg Becker. 

The Relation of Parasitic Amebae to Disease 150 

Capt. Charles F. Craig. 

The Identification of the Pathogenic Entameba of Panama 168 

Dr. S. T. Darling. 

List of Parasitic Amebae, arranged alphabetically 179 

Howard Crawley. 

Der Kernaufbau der parasitischen Amoben 185 

Dr. M. J. S. von Prowazek. 

Compendium of all Amebae, arranged according to their Hosts, Regard- 
less of the Zoological Status of the Species of Amebae 194 

Albert Hassall. 

Bibliography of Parasitic Amebae 198 

Albert Hassall. 

Genera and Species of Ameba 287 

Dr. Gary N. Calkins. 

The Cultivation of Amebae 305 

Dr. Gary N. Calkins. 

The Relation of Anaphylaxis to Immunity and Disease 311 

Prof. Victor C. Vaughan. 

Studies on the Locus of Antibody Formation 328 

Drs. Frederick P. Gay and G. Y. Rusk. 

On the Mechanism of Intoxication in Pneumococcus Anaphylaxis and in 

Pneumococcus Infections 338 

Dr. E. C. Rosenow. 



Transfer of Immunity through Colostrum 342 

Dr. L. W. Famulenee. 

Anaphylactic Reaction in Pellagra Patients, by the Inoculation of Watery 

Extract of Spoiled Maize 344 

Guido Volpino. 

Zur Frage der Paratyphus-Erkrankungen 347 

Dr. Simon von Unterberger. 

Index 683 

Joint Sessions of Sections I and V, and of Sections I and VIII, are found in 

Volume I, Part II. 



66602— vol 2, pt 1—13 1 


Prof. Theobald Smith, President Section /, 

Fifteenth International Congress on Hygiene and Demography. 
Sir : In accordance with the provision of Article XII of the regu- 
lations of the congress, we herewith submit a report of the section pro- 
ceedings of the meeting held at Washington, September 23 to 28, 
1912, together with such manuscripts of the papers read as have been 
delivered into our hands as secretaries pro tempore, Dr. Philip Han- 
son Hiss being unavoidably absent. 

Monday, September 23 — 3 p. m. 

The first session was called to order by the president, Prof. Theo- 
bald Smith, who announced the following honorary presidents of- 
Section I: 

Prof. Friedrich Loeffler, of Greifswald, Germany; Prof. August 
Gaertner, of Jena, Germany ; Prof. George Nuttall, of Cambridge, 
England; Prof. Adolf Dieudonne, of Munich, Germany; Regie- 
rungsrat Dr. A. Weber, of Berlin, Germany ; Prof. Alfred Petters- 
son, of Stockholm, Sweden; Prof. Karl Landsteiner, of Vienna, 

Dr. D. L. Harris, nominated by Dr. V. C. Vaughan, was made tem- 
porary secretary. 

Papers were presented in the symposium on filterable viruses as 
follows : 

Some Experiments upon the Nature of the Virus of Rabies, 
by Drs. Daniel Warren Poor and Edna Steinhardt, Department 
of Health, New York City. 

Natural and Induced Immunity to Typhus Fever, by Drs. 
Goldberger and Anderson, United States Public Health Service, 
Washington, D. C. 

Observations on a Chicken Sarcoma and its Filterable Cause, 
Drs. Rous and Murphy. 

Tuesday, September 24 — 9.30 a. m. 

The second session was called to order hy the president, Prof. 
Theobald Smith, who presided throughout the morning. 



Papers were presented on the subject of special selective media for 
microorganisms, as follows: 

Selective Culture Media for Growth of Cholera Spirilla, by 
Prof. Dr. Adolf Dieudonne, University of Munich, Germany. 

Egg Agar as Culture Medium for Cholera Spirilla, by Dr. 
Charles Krumwiede, jr., New York City. 

A Plating Medium for the Recognition of Acid and Nonacid 
Producing Bacteria, by Dr. A. J. Bendick, College of Physicians 
and Surgeons, Columbia University, New York City. 

Special Culture-media for Pure Cultures of Amebae found in 
Intestines of Animals, Dr. A. W. Williams, research laboratory, 
New York City. 

Bacterial Water Examination, by Prof. Edwin O. Jordan, 
University of Chicago, Chicago, 111. 

Cultivation of Malarial Plasmodia in Vitro, by Dr. C. C. Bass, 
New Orleans, La. This subject was illustrated with lantern 
The following members of the congress joined in the discussion : 

Dr. E. Libman (New York City), Dr. Karl Landsteiner 
(Austria), Capt. C. F. Craig, U. S. Army (Washington, D. C), 
Prof. Dr. A. Gaertner (Jena, Germany), Dr. F. L. Rector 
(Brooklyn, N. Y.), Prof. Edwin O. Jordan (Chicago, 111.), Dr. 
Wm. H. Park (New York City). 

Tuesday, September 24 — 2.10 p. m. 

The third session was called to order by the president, Prof. Theo- 
bald Smith, who presided throughout the afternoon. 
Papers were presented upon miscellaneous subjects, as follows: 

A Critical Study of Acid-fast Bacilli Cultivated from the 
Human Leprous Lesion, with Especial Reference to their Etio- 
logical Significance, by Prof. Charles W. Duval, Tulane Uni- 
versity, New Orleans, La. 

Influenza Meningitis, Experimental and Clinical, by Dr. 
Martha Wollstein, Rockefeller Institute for Medical Research, 
New York City, was read by title, its author being absent. 

Preventive Inoculations: Experimental and Clinical Studies 
on the Use of Leukoc}'tic Extract in the Treatment of Erysipelas, 
Pneumonia, et cetera, by Prof. Philip Hanson Hiss, jr., Columbia 
University, New York City. (Read by Dr. W. H. Park.) 

The Production of Antirabic Immunity by Intraspinal Injec- 
tions of Virus, by Dr. D. L. Harris, Bacteriologist to Hospital 
Department, St. Louis, Mo. 

The Etiology of Trachoma, by Dr. Anna W. Williams, Re- 
search Laboratory, Department of Health, New York City. 


The following members of the congress took part in the discussion : 
Dr. C. Wellman (New Orleans, La.), Dr. Libman (York City), 
Dr. Karl Landsteiner (Austria). 

Wednesday, September 25 — 9.30 a. m. 

The fourth session was called to order by the president, Prof. 
Theobald Smith. 

Papers were presented upon the topic of paratyphoid and para- 
typhoidlike bacilli with especial reference to their dissemination in 
nature and their relation to man and animals as follows: 

A Report of Work Done at the Kaiserlichen Gesundheitsamt, 
by Regierungsrat Prof. Dr. A. Weber, Berlin, Germany. 

Studies on Typhoid and Paratyphoid Organisms at the Lister 
Institute. Dr. J. Henderson Smith, Lister Institute, London, 

Paratyphoid and Allied Bacilli, including the Bacteriology of 
Animal Foods, by M. le Dr. Sacquepee, Prf. au Val-de Grace, 
Paris, France. 

Representatives of the Gartner Group Isolated from the 
Tissues of Laboratory Animals, by Dr. John C. Torrey, Cornell 
University Medical College, New York City. 

A Bacteriological Examination of Market Milk, by Dr. P. G. 
Heineman, University of Chicago, was read by title, its author 
being absent. 
The following members of the congress joined in the discussion : 
Dr. Wm. H. Park (New York City), Dr. W. Fornet (Berlin), 
Dr. E. Libman (New York City), Prof. C. E. A. Winslow (New 
York City), Dr. William H. Welch (Baltimore, Md.). 

The recommendation for an international commission to prepare a 
standard of procedure for determining B. Coli, as suggested by Dr. 
Weber, was then considered by the section. 

Prof. William H. Welch moved that a committee be established, 
with Dr. Weber as chairman, and that members be added as the 
commission desired. This motion, while not acted upon at this 
time, was assented to by the leading members of the section, and was 
forwarded to the Permanent International Commission. 
The following additional papers were then read: 

La Tuberculosis Experimental en las Grandes Alturas, by Dr. 
Nestor Morales. 

Milzbrand und Salvarsan, Dr. Geo. Becker, Plauen, Germany. 

Thursday, September 26 — 9.15 a. m. 

The section joined with Section V in a symposium on poliomyelitis, 
etiology, and mode of transmission. 

Dr. Hermann M. Biggs, president of Section V, presided. 


The following papers were presented: 

Epidemic Poliomyelitis in Norway, by Prof. Dr. Francis 
Harbitz, Koneglige Frederiks Universitet, Christiania, Norway. 
Sanitary Measures against Poliomyelitis, by Privat-Docent Dr. 
Karl Landsteiner, k. k. Universitat, Vienna, Austria, and Dr. 
Simon Flexner, Rockefeller Institute for Medical Research, New 
York City. 
N The Etiology of Poliomyelitis and Prophylactic Measures, by 

M. Neustaedter, M. D., Ph. D., instructor in neurology, iS'ew 
York University and Belle vue Hospital Medical College, New 
York City. 

Ueber die Verbreitungsweise der epidemischen Kinderlahmung 
und die Verhiitung ihrer Verbreitung, by Prof. Alfred Petters- 
son, Stockholm, Sweden. 

Die histologischen Veranderungen im Riickenmarke des Affen 
bei experimenteller Poliomyelitis, by Prof. Alfred Pettersson, 
Stockholm, Sweden. 

Einige epidemiologische Beobachtungen bei der Kinder- 
lahmungsepidemie in Schweden, 1911-1912. Kurzes Resume, by 
Prof. Alfred Pettersson, Stockholm, Sweden. 

Anterior Poliomyelitis, as observed in Massachusetts, 1907- 
1911, by Dr. Mark W. Richardson, Secretary State Board of 
Health, Boston, Mass. 

A Preliminary Announcement of Observations on the Role of 
Stomoxys Calcitrans in the Spread of Anterior Poliomyelitis, 
by Prof. M. J. Rosenau, Harvard University, Boston, Mass. 
The following members of the congress joined in the discussion: 
Prof. Geo. Nuttall (Cambridge, England), Prof. Dr. Friedrich 
Loeffler (Germany), Dr. Karl Landsteiner (Vienna, Austria), Prof. 
A. Pettersson (Stockholm, Sweden), Prof. W. S. Thayer (Baltimore, 
Md.), Dr. Francis E. Fronczak (Buffalo, N. Y.), Dr. M. J. Rosenau 
(Boston, Mass.), Dr. Frankl-Hochwart (Vienna, Austria). 

Thursday, September 26 — 2.15 p. m. 

The fifth session was called to order by Prof. Charles W. Stiles. 
The following papers were read : 

The Relation of Parasitic Amaebae to Disease, by Capt. 
Charles F. Craig, United States Army, Washington, D. C. 

The Identification of the Pathogenic Entameba of Panama, 

by Dr. Samuel T. Darling, Ancon Hospital, Ancon, Canal Zone. 

Nomenclature of Genera and Species of Amebae, by Howard 

Crawley, zoological division, Department of Agriculture, Wash- 

. ington, D. C. 


Present Status of Knowledge of Structure of Nucleus of all 
Known Parasitic Amebae, by Dr. M. J. S. von Prowazek, See- 
mannskrankenhaus und Institut fur Schiffs- und Tropenkrank- 
heiten, Hamburg, Germany, was read by title, its author being 

Compendium of all Amebae, Arranged According to their 
Hosts, Regardless of the Zoological Status of the Species of 
Amebae, by Albert Hassall, assistant zoologist, United States 
Department of Agriculture, Washington, D. C. 

Bibliography of Parasitic Amebae, by Albert Hassall, assist- 
ant zoologist, United States Department of Agriculture, Wash- 
ington, D. C. 

Present Status of Zoological Classification of the Parasitic 
Amebae (Genera and Species) ; also Present Status of Technique 
in Studying Amebae (Free and Parasitic), by Prof. Gary N. 
Calkins, New York City, were read by title, their author being 
The following members of the congress joined in the discussion: 
Dr. C. Wellman (New Orleans, La.), Dr. Charles F. Craig (Wash- 
ington, D. C), Dr. Samuel T. Darling (Ancon, Canal Zone). 

Friday, September 27 — 9.30 a. m. 

The sixth session was called to order by Prof. Theobald Smith. 
Papers were presented in the symposium on anaphylaxis, as 
follows : 

The Relation of Anaphylaxis to the Infectious Diseases, by 
Dr. Victor C. Vaughan, University of Michigan, Ann Arbor. 

Studies on the Locus of Antibody Formation in the Animal 
Body, by Dr. Frederick P. Gay, University of California, 

Pneumococcus and Anaphylaxis, by Dr. Edward C. Rosenow, 
Memorial Institute for Infectious Diseases, Chicago, 111. 

Transfer of Immunity through Colostrum, by Dr. L. W. 
Famulener, Research Laboratory, Department of Health, New 
York City. 

Anaphylactic Reaction in Pellagra Patients by the Inoculation 
of Watery Extract of Spoiled Maize, by Mr. Guido Volpino. 

Zur Frage der Paratyphus-Erkrankungen, von Dr. S. von 
Unterberger, St. Petersburg. 

Phenomena of Anaphylaxis in Pellagra Patients Inoculated 

with a Watery Extract of Spoiled Maize, by Prof. L. Pagliani, 

Turin, Italy. 

The following members of the congress joined in the discussion: 

Dr. Wm. H. Park (New York City), Prof. Frederick P. Gay 

(Berkeley, Cal.), Dr. A. D. Hirschfelder (Baltimore, Md.). 


The president, Prof. Theobald Smith, declared the section ad- 
journed, since the further proceedings of the section would be merged 
with those of Section VIII. 

Friday, September 27 — 2 p. m. 

A joint session of Sections I and VIII. The session was called to 
order by Dr. Henry G. Beyer, the president of Section VIII. 

The following papers were presented on the general subject of 
hookworm and hookworm diseases: 

Biologie de l'Ankylostoma Duodenale Dubini, par les Drs. M. 
Breton et L. Bruyant (Institut Pasteur de Lille). 

Number of Treatments and Number of Full Doses of Thymol 
Administered in 61 Hospital and 22 Home-cured Cases of Hook- 
worm Infections, by Dr. Charles Wardell Stiles, professor of 
zoology, and George F. Leonard, first assistant, Hygienic 
Laboratory, United States Public Health Service. 

Proportion of Males to Females in the American Hookworm 
(Necator americanus), Based on 13,080 Hookworms from 102 
Cases, by Dr. Charles Wardell Stiles, professor of zoology, and 
W. L. Altman, assistant, Hygienic Laboratory, United States 
Public Health Service. 

Der Infektionsweg bei Strongyloides und Ankylostomum, 
von Prof. Dr. F. Fulleborn, Hamburg. 

Das Oleum chenopodii anthelmintici gegen Ankylostomiasis 
im Vergleich zu anderen Wurmmitteln, von Dr. W. Schuffner 
und Dr. H. Vervoort, Leipzig-Borsdorf. 

Uncinariasi od Anchilostomiasi, by Prof. E. Perroncito, Turin. 
Control and Eradication of Hookwork Disease, by Maj. Baily 
K. Ashford, United States Army. 

Distribution of the Hookworm Disease, by Dr. W. S. Eankin, 
Ealeigh, and Dr. Hiram Byrd, Jacksonville. 

Methods for the Eradication of Hookworm Disease, by Dr. 
John A. Ferrell, Ealeigh. 

A Study of the Hemoglobin in its Eelation to the Number of 
Hookworms Present, by C. W. Stiles and George A. Wheeler. 
The following members of the congress joined in the discussion: 
Dr. W. H. Schultz (Washington, D. C), Dr. Claude A. Smith 
(Atlanta, Ga.), Dr. Charles W. Stiles (Washington, D. C), Dr. S. T,* 
Darling (Ancon, Canal Zone). 

Eeports of discussions as given to the secretary will be found in 
the transactions of this section. 

Dr. D. L. Harris, St. Louis, Mo. 
Dr. F. M. Meader, Syracuse, N. Y. 




By Dr. Daniel Warren Poor and Dr. Edna Steinhardt, Department of Health, 

New York City. 

Most of the experimental work on rabies has been with the virus 
as it occurs in the brain and spinal cord. In this situation it is 
closely associated with the elements of the nerve tissue. Compara- 
tively little has been done with the virus as it occurs in the salivary 
glands, where it is presumably in a more or less free state. In our 
work, which has been confined to the gland virus almost exclusively, 
we had two objects in view. First, that of determining, in a measure, 
to what extent the association of the nerve tissue affected the various 
physical tests for determining the nature of the virus, and, second, 
that of comparing the physical properties of the virus in the two situ- 
ations; this with the idea of noting any differences which might be 
found suggestive of the parts of a cycle. 

Two methods have been used for obtaining the virus, the sub- 
maxillary glands from the carcasses of dogs brought to the laboratory 
with clinical rabies being used in both instances. In the first method, 
after removal of the fibrous sheath, the glands were immersed in 
sterile neutral glycerin and allowed to stand in the ice-box for from 
6 to 12 days. Although virus may be extracted from the intact 
glands, it was found that more was removed when the glands were cut 
in pieces with a sharp razor or scissors. The clear supernatant 
glycerin, slightly colored by hemoglobin, is then pipetted off. This 
is usually found to be sterile. The glycerin containing the virus i« 
next placed in collodion sacs and the glycerin removed by dialysis 
in running physiological salt solution. One and a half hours are 
usually sufficient for the removal of the glycerin from 4 or 5 c. c. 
of the glycerin virus. In this way it is possible to obtain a sterile 
suspension of the virus in physiological salt solution. Microscopical 
examination of this fluid shows it to be an exceedingly clear liquid 
with practically nothing demonstrable in the way of formed cellular 
elements. Virus obtained in this manner will subsequently be re- 
ferred to a glycerin-extract virus. 

In the other method the glands, after being cut, are placed in dis- 
tilled water and subjected to a vacuum of 29 inches of Hg for an 



hour. The pieces of the glands were then placed in an ordinary 
meat press and the remaining fluid pressed out. This is centrifuged 
and the supernatant fluid added to the water in which the glands were 
aspirated. It may be noted that the aspiration fluid alone was 
found to contain the virus, but more was present on the addition of 
the pressed-out juice. By this method a suspension of the virus is 
obtained in distilled water which is stronger than the glycerin virus, 
but which is not sterile and which contains fragments of gland cells, 
blood cells, etc. Subsequent experiments showed that bacteria and 
formed tissue elements could be removed by passing it through a 
Berkefeld filter. This virus will be referred to as aspiration virus. 

That the virus in the central nervous system is in a less extractible 
or less free condition than in the glands would appear from the 
following observation : 

Glycerin extracts of the glands of 32 dogs whose brains were posi- 
tive to the Negri test were virulent in 71 per cent of the cases. 

Eleven fixed virus brains, similarly tested, gave virulent extracts in 
only 36 per cent of the cases, and four street virus brains were all 
nonvirulent. When one considers that the brain is the culture me- 
dium for the rabies organism, which is present in much greater num- 
bers in this. situation than in the glands, one would expect a greater 
number of virulent brain extracts unless, as is undoubtedly the case, 
the virus is intimately associated with the nerve cells. Indeed, the 
virulent extracts from the brain virus might be accounted for by 
minute particles of the brain substance being torn off by the action 
of the glycerin (the brain being a more delicate tissue than the 
gland), or by the extraction of the virus from the blood and lym- 
phatic vessels and spaces. 

That the action of the glycerin on the glands is mainly that of a 
sucking out of the virus from the tubules is seen from the following 
experiment: The glands from two rabid dogs, which had given a 
nonvirulent glycerin extract, were removed from glycerin and ground 
up in a mortar with salt solution, a difficult operation owing to the 
tough and slippery constitution of the gland. This emulsion proved 
to be quite virulent. On the other hand, in some glands much virus 
was present in the ducts, as it was possible by a second extraction 
with fresh glycerin to remove virus which produced rabies with a 
short incubation. 


In 1903 Remlinger 1 first showed that fixed virus was filterable. 
He emulsified the entire brain of a fixed virus rabbit in 400 c. c. of 
water and filtered the emulsion through a Berkefeld V under pres- 
sure. Ten rabbits were inoculated with from \ to 1 c. c. each of the 
filtrate. Three of these rabbits, or 30 per cent, developed rabies. 

Poor and 1 
Stein liardt. J 



The following year, Marie, using three different Berkefeld candles, 
was unable to pass the virus through in any instance. In the same 
year (1904), however, Bertarelli and Volpino 2 successfully filtered 
fixed virus through a Berkefeld V five times out of seven trials. 
They failed, however, to pass it through a Chamberland F. Celli 
and Du Blasi * had similar results. In 1904, also, De Vestea 4 made 
extensive experiments on filtration. He used fixed virus, and pre- 
pared the emulsions with great care, emulsifying the brains with 
the aid of quartz sand. He filtered with from two to three atmos- 
pheres pressure, and inoculated his animals with lai*ge amounts of 
the filtrate, i. e., | to 1 c. c. each. His results were as follows : 



Per cent. 

Berkefeld V 







Berkefeld N._ 

i 7u 

Chamberland F 


Chamberland B (filtrate from Chamberland F) 

Maason filter (filtrate from Berkefeld) 

The literature contains very little regarding the filtration of gland 
virus. In one instance, a virulent filtrate was obtained by Berta- 
relli and Volpino, who passed it through three layers of paper. It 
is also recorded that the virus in human saliva was passed in one 
instance through a Berkefeld candle. 

Our experiments were made with Berkefeld V and N, Chamber- 
land F and B, and with a collodion filter. The aspiration virus 
from the glands of from two to four dogs were used in each experi- 
ment. The results were as follows: 




Berkefeld V _ _.. 






) ,™ 

Berkefeld N 


Chamberland F 


Chamberland N 


In the collodion and the first Chamberland B experiment the virus 
used unfortunately proved to be qifite weak. In the second Chamber- 
land B experiment, however, a strong virus was obtained and the 
animals inoculated with the filtrate failed to show symptoms of 
rabies after a lapse of 6 weeks. 

In order to get some idea of the amount of virus held up by the 
filter a series of dilutions of the fluid to be filtered w T as made as 
follows : Dilutions of 1 to 4, 1 to 8, 1 to 10, 1 to 20, and 1 to 30. It 
was found that the average incubation of the guinea pigs inoculated 
was increased in a surprisingly regular manner according to the 
degree of the dilution of the virus. For example, the dilution of 


1 to 4 gave an incubation of 9 J days, as against 8| days for the un- 
diluted virus, an increase of § day only. A dilution of 1 to 30 gave 
an incubation of 10^ days, as compared with 8 days for the original 
virus, an increase of 2J days. The average duration of incubation, 
then, may be taken as a rough index of the dilution of virus. All 
of the guinea pigs inoculated with the Berkefeld filtrates developed 
rabies. That more of the virus passes through after saturation of 
the filter is seen from the following experiment: A small Berkefeld 
V candle was used. The first 5 c. c. which passed constituted the first 
filtrate, the next 12 c. c, the second filtrate. The four guinea pigs 
inoculated with the first filtrate developed rabies with an average 
incubation period of 21 days. Those inoculated with the second 
nitrate developed in 12J days. Those with the unfiltered material, 
diluted eight times, developed in 9^ days and, with undiluted con- 
trol, in eight days. Comparing the incubation of the pigs injected 
with the second nitrate, 12^ days, with that of the pigs injected with 
the control diluted 1 to 8, 9J days, it is fair to assume that in this 
case the virus was diluted by filtration more than eight times. Again 
in the finer Berkefeld, grade N, the average incubation of the pigs 
injected with the second filtrate was 15 J days, and that produced by 
the virus diluted 1 to 20, was only 11J days. In a further attempt 
to determine the dilution caused by filtration, a Berkefeld V candle 
was shaved to about one-half its thickness. In this case, a weak 
virus, diluted 1 to 20, gave an incubation of IT days; while the fil- 
trate from the shaved filter gave 16 days, practically the same, so 
that it may be assumed that the shaved filter diluted the virus about 
20 times. The filtrates from the Chamberland filters gave corre- 
spondingly increased incubation. Thus, in one test, two out of four 
pigs ^inoculated developed rabies with an average incubation of 33 
days, as against 8 J days for the control. In a second test, two out 
of five pigs developed, with an average incubation of 47 days, as 
against 11 days for the control. The filters were tested with a sus- 
pension of pyocyaneus bacilli, which was mixed with the virus to be 
filtered. In no case did the bacilli pass through. Comparing now 
our results with the filtration of gland virus with those obtained by 
others in the filtration of the fixed brain virus one may infer that 
the greater regularity with which the gland virus passes (that is 
100 per cent in the Berkefeld as against 75 per cent, and 75 per cent 
in the Chamberland F as against 25 per cent obtained by De Vestea) 
is due to the freer condition of the virus as appearing in the glands. 
That the organism is not necessarily smaller in this location is seen 
from the fact that the fixed virus did pass the Chamberland filter 
and. even in one instance, according to De Vestea, the Maasen filter. 
When one considers further the greater number of organisms in fixed 
virus, the greater c:\re used by De Vestea in preparing his emulsions, 

StelnharV ] THE VIRUS 0F BABIES. 13 

i. e., the grinding up with quartz sand and the larger amount in- 
oculated in his animals, J to 1 c. c., as against \ to J c. c., in our 
animals, the above conclusion seems all the more apparent. Whether 
this would indicate that the central point of the Negri body may be 
the true rabic parasite — the outer portion being a degeneration 
product of the nerve cell — we are at present unprepared to say. The 
following points are to be considered in this connection: First, the 
structure known as the complete Negri body could not pass the 
filter. Second, some of the minute inner cell structures might pass 
through. Third, these small central structures might easily exist 
free in the glands and escape identification. In this connection, it is 
interesting to note that, working in conjunction with Dr. Robert 
Lambert, we have been able to produce inclusions closely resembling 
the outer portion of Negri bodies, by allowing normal nerve cells to 
slowly degenerate in plasma at 37° C, according to Harrison's 
technique for the growing of tissues. 


In the first method tried, the spinal cord of a fixed virus rabbit 
four days after subdural inoculation was used. At this time the virus 
has reached the cervical end, but has not extended to the lumbar 
extremity. The cord was quickly removed from the canal by the 
Oshida method, and blocked into previous sterilized paraffin of 46° C. 
melting point. The whole block was then immediately solidified in 
ice water. In this way a more nearly anaerobic condition was ob- 
tained, a condition considered by Marie to be desirable. At the end 
of 10 days, not only had the virus not extended to the lower end, but 
had died out in the cervical end. 

Attempts were then made to grow the virus, or at least to get a 
line on its viability by making use of the technique of Harrison's 
method of tisue growing. It was found that apparently the brain 
cells retained their vitality at incubator temperature for several 
days; in one distance as long as 21 days. This was inferred from 
the perfect staining of the Nissl bodies. However, in spite of the 
ganglion cells remaining alive, small portions of the fixed virus 
brains embedded in plasma, agar, and in simple saline solution, lost 
their virulence after seven days at 37° C. 

On the other hand, in the only instance in which street virus brain 
was tried, it was found that the virulence was retained after eight 
days at 37° C. 

Portions of normal guinea pig brain inoculated with weak emul- 
sion of fixed virus showed no virulence after six days. Normal brain 
was also in a similar manner inoculated with gland virus, but here 
also there was no evidence of virus at the end of six days. Unfor- 
tunately, in this experiment a glycerin extract virus was used which 


proved to be very weak* From our subsequent work, as will as from 
clinical observations, we would conclude that the most promising 
virus to use for this purpose, would be the strong aspiration virus 
freed from bacteria by passage through a Berkefeld filter. This 
would avoid the objection to brain virus for the cultivation of the 
rabic organism, made by Marie, 5 on the ground that at incubator tem- 
perature the brain tissue develops substances detrimental to the 


The glycerin extract dialyzed in distilled water or in salt solution, 
even after concentration through a collodion sac, gave a product 
which, while containing the organism, showed remarkably little in 
a way of formed elements of any kind. The aspiration virus, when 
filtered through a Berkefeld candle, showed many small granules, 
evidently from the secreting cells of the glands. Both of these 
viruses were examined with the dark field (1/12 and 1/16 lenses and 
Xo. 4 ocular) and in the preparations stained by Giemsa's stain. 

Although very minute granules were found, Ave were unable to 
identify them as organisms. 

An attempt was made to agglutinate the granules with an antirabic 
serum but without definite result. 


These two viruses were compared, with the idea of noting any 
difference that might exist suggestive of a different physical form in 
the two situations. The tests were made with reference to the effect 
of (1) Eapid drying; (2) Drying and heat ; (3) Heat; (4) The effect 
of certain chemicals ; (5) Viability; (6) Dialysis. 

(1) Rapid drying. — It has been known for some time that brain 
virus could be dried rapidly and retain its virulence, but it has been 
quite generally supposed that the gland virus rapidly lost its virulence 
upon drying. 

An emulsion of brain virus made with distilled water and dialyzed 
for two hours was spread in a thin layer and dried in a vacuum 
of 29 inches Hg over H 2 S0 4 . After 16 hours it was completely 
dried. Inoculated into guinea pigs, it produced rabies in five to 
six days, the same as in the control kept in the ice box. The same 
technique, applied to two aspiration gland viruses in distilled water 
from two different dogs, produced a like result, the pigs inoculated 
from this dried virus contracting rabies in nine and one-half days 
identically with the controls. 

(2) I>i>jing and heat. — This emulsion of fixed virus and a sample 
of glycerin gland virus were dialyzed in distilled water for an hour. 
Very thin layers oi eatih were evaporated to dryness while exposed 

Steinlmrdt. ] THE VIRUS OF RABIES. 15 

to 37° C. for (5 hours. In each case the virus was killed while the 
controls were fully virulent. 

(3) Heat. — Thermal death point: 

10 minutes. 
i hour 

10 minutes. 
$ hour 

F. V. weakened. 

Gl. V. weakened. 

F. V. very much weakened, only one out of three animals 

Gl. V. killed. 

60° 0. 

F. V. exper. lost through disappearance of the animals. 
Gl. V. killed. 
F. V. killed. 
Gl. V. killed. 

(4) Effect of chemicals. — A 1-1000 solution of HgCl 2 apparently- 
killed both viruses. 

A 1-1000 solution of HC1 killed the brain virus and markedly 
weakened the gland virus, only one pig out of three contracting rabies 
with a prolonged incubation. Mg0 2 , in the strength of \ gm. to 
4 c. c. of the virus, produced but little effect on either virus. 

(5) Viability. — Gland virus aspirated in distilled water was kept 
in an ice box at 45° F. for 15 days, at the end of which time it had 
become offensive through bacterial contamination. It was then fil- 
tered through a Berkefeld V candle, a filtrate being obtained which 
produced rabies with an incubation of 14 days. This filtrate was 
then kept at room temperature arid exposed to the light for 45 hours. 
At the end of this time the virulence was completely lost. An emul- 
sion of fixed virus in distilled water, exposed to the same conditions 
for the same length of time, was markedly weakened, the incubation 
of the injected animals being increased to 10 days, i. e., five days 
longer than the controls. Exposure to light and room temperature 
for four days destroyed the virulence of the brain emulsion. This 
experiment gives but a rough comparison, as there were undoubtedly 
many more organisms present in the fixed virus emulsion than in the 
gland virus filtrate. In another experiment, the Berkefeld filtrate, 
from an aspiration gland virus kept in the ice box for nine days, had 
lost its virulence, while the unfiltered virus, kept in the same manner 
for the same length of time and then filtered, was shown to be viru- 
lent. This is in accord with the experiments of De Vestea on brain 
virus. He found that the filtrate of fixed virus died out in the ice 
box within a week, while the original retained its strength for a 
long time. 

(6) Dialysis through the collodion sac. — Novy has shown that 
dialysis kills fixed rabic virus apparently through the extraction of 
certain salts and that the time required depends on certain factors, 
such as the thickness of the emulsion, rate of flow of the water, etc. 


Our results were similar to his, though not identical with them, 
probably owing largely to the fact of our using much stronger 

We found, e. g., that the dialysis of 2 c. c. of either brain or gland 
virus in 200-300 c. c. of standing water had but little effect after 18 
hours, but that dialysis of the gland virus in running water for 18 
hours killed it. Brain virus, on the other hand, while it was 
markedly weakened, was not completely killed. Dialysis for 42 hours 
killed the fixed virus emulsion used by us. In the dialysis experi- 
ment, there were many more tissue elements, as well as organisms, in 
the brain virus emulsion used, than in the glycerin extract gland 
virus, which undoubtedly accounts for the longer time required for 
killing the former virus. 

An interesting reverse experiment was the following : 

Some of the filtrate from a Berkefeld V candle was evaporated in a 
vacuum over H 2 S0 4 to one-fifth its bulk, the operation requiring 
four hours. The control, in a narrow tube sealed with paraffin, was 
placed in the apparatus so that conditions of light and temperature 
would be the same. Three guinea pigs were inoculated from the con- 
centrated virus, as well as the control, and also the concentrated virus 
diluted to its original volume. The result was that while the pigs 
inoculated with the control died with an average incubation of 19 
days, those from the concentrated virus developed only after a period 
of 30 days, while only one pig from the concentrated virus subse- 
quently diluted developed after 19 days. 

This suggests a harmful concentration of salts such as is believed 
by Harris 6 to cause the reduction of virulence in the Pasteur cords. 


In conclusion, we wish to emphasize the following points : 

(1) The advantage of using the gland secretions in the study of 
rabies, for the reason that they contain the organism in a condition 
freed from tissue cells. This is an advantage for the microscopical 
study of the virus ; for the study of its physical properties, and for its 
use in growing experiments. 

(2) The two easy methods for obtaining bacterially sterile virus 
from the glands. 

(3) The regularity with which the gland virus passes the filters. 

(4) The similarity in the nature of rabies virus in the two locations 
of the brain and the glands. 

1 Remlinger, Annal. de l'lnstitut Pasteur, 1903. 

"Bertarellj and Volpino, Riv. d'Ig., 15, 190L 

3 CelJi and du Blasl, Annal. d'Ig. Speriment, 1904. 

4 De Vestea, La Med. Ital., 1904, No. 13, and Annal. d'Ig. Speriment, 1905. 

5 Marie, L' Etude Experimental de la Rage. (Doin et fils, Paris, 1909.) 
* Harris, Journal of Infectious Diseases, May, 1912. 

GolS°ger and ] IMMUNITY TO TYPHUS. 17 


John F. Anderson, Director Hygienic Laboratory, and Josei>ii (Joi.duebgeb, 
Passed Assistant Surgeon, United States Public Health Service, Washington, 
D. C. 

Instances of transient or even permanent natural immunity of 
human beings to certain infections are not unknown. Most of these 
are clinical observations. It has been frequently noted that of a num- 
ber of persons of a family or of a community presumably equally 
exposed some escape. Those who have made many vaccinations for 
the prevention of smallpox, especially of children, are familiar with 
the fact that sometimes an individual may resist several repeated 
inoculations; this, while it may frequently be attributed to a non- 
potent virus, is in some instances at least undoubtedly due to a more 
or less transient natural immunity to vaccinia. 

An interesting instance of natural immunity to an infectious dis- 
ease in the human subject is reported by Reed (1901). One of the 
subjects experimented upon by Reed and Carroll resisted a subcu- 
taneous injection of 1.5 c. c. of yellow-fever blood, and later also the 
bites of some infected mosquitoes. 

Similar examples of individual resistance of animals to experi- 
mental infection have been noted. In the course of our studies on 
measles we found quite a marked variation among monkeys in the 
susceptibility of different individuals to the disease. Marks has 
well brought out the variation in susceptibility of young rabbits to 
poliomyelitis; and Dorset, McBride, and Niles report instances of 
natural immunity in the hog to hog cholera. Metchnikoff and Bes- 
redka (March, 1911) report that in one of 16 experiments they 
failed to infect the chimpanzee with typhoid, and McCoy and Chapin 
(January, 1911) report that a considerable percentage of San Fran- 
cisco rats were found by them to be immune to plague at a time 
when immunity, due to a previous attack, could reasonably be ex- 
cluded. Coming to typhus, we find that Nicolle was unsuccessful in his 
initial attempts to infect monkeys directly from the human subject, 
and from his experience concluded that to obtain success the virus 
had to be prefaced by passage through a higher ape, the chimpanzee. 

Our own work and that of Ricketts and Wilder, of Gavino and 
Girard, and others, and more recently that of Nicolle himself, has 
shown that such prefatory treatment of the virus is unnecessary. 
The apparently ready susceptibility of the monkey encountered by 
us in our early work suggested to us that Nicolle's initial lack of 
success was due to the small amount of blood used, to the subcutaneous 
route employed by him in those inoculations, or to both combined. 
66692— vol 2, pt 1—13 2 


Apart from these factors there appeared to us no reason to sus- 
pect natural resistance as playing a part in explaining Nicolle's 
negative results. 

Gaviiio and Girard appear to have been the first to suggest that 
some monkeys may be naturally immune to typhus. They reported 
that a monkejr of the species Ateles vellerosus that had previously 
received an injection of heated typhus blood failed to present any 
reaction following an immunity test of 3 c. c. of blood virulent for 
the control. They suggest that instead of the animal having been 
vaccinated by the first noninfecting injection it may have been nat- 
urally immune to typhus. 

Dreyer (1911) reports that in the course of his work he found one 
monkey (Cercopithecus?) entirely refractory. This animal showed 
no trace of illness, although two others treated with the same ma- 
terial at the same time and in substantially the same dose promptly 
developed the usual (typhus) symptoms. He believed himself quali- 
fied in interpreting this as a case of natural immunity. He does not 
state whether he tested the susceptibility of this animal a second time. 

Wilder reports that a monkey that had received an injection of 
filtered typhus-blood serum failed to react when given an immunity 
test of 4 c. c. of typhus virulent blood and suggests, among other 
possibilities, that the animal may have been naturally immune. 

Nicolle and his coworkers, in their interpretations, do not appear 
to have considered the possibility of a natural immunity in the 
monkey ; we believe, however, that a critical study of their reported 
protocols shows that they had encountered the same phenomenon. 
We believe, however, that a critical study of their reported protocols 
shows that they had encountered the same phenomenon. 

In the course of our recent work with the New York and the 
Mexican virus we obtained results that brought the possibility of the 
occurrence of a natural resistance to typhus forcibly to our attention. 

We have summarized all our monkey inoculations in which the 
first or primary inoculation was with monkey typhus blood. The 
virulence of the blood used and the dose, as well as the route of 
inoculation employed, unless otherwise stated, was always proven. 
It was found that 46 monkeys were given a primary inoculation of 
virulent defibrinated blood and to this 8, or 17.4 per cent, failed to 
react. These 8 were given a second inoculation, to which 4, or 8.7 
per cent, of the original 40 failed to respond. It is proper to state, 
however, that one of these 4 may perhaps be considered to have pre- 
sented a slight suggestion of an " abortive " reaction— so slight, how- 
ever, that it escaped our attention at the time of its occurrence. If 

i;!ll%MTS.r! n(] ] IMMUNITY TO TYPHUS. 19 

we count this as a positive reaction, we have only 3 of the 8 that 
failed to respond to a second inoculation ; or, in other words, at least 
6.5 per cent of the monkeys failed to respond to two separate inocu- 
lations with virulent blood. 

Of the three clearly resistant to the second inoculation, the im- 
munity of only two was further tested; of these, one — rhesus No. 
197 — although given less than half its previous dose now developed 
a mild though well-defined febrile reaction ; the other, rhesus No. 
189, presented no indication of a reaction. After this, rhesus No. 
189 was subjected to five more tests. In all, between January 2 and 
June 29 this animal received 8 inoculations with virulent blood, 
ranging in amount from 3 to 14 c. c., to which no recognizable evi- 
dence of a reaction was noted at any time during the period of 

Of 46 animals, therefore, one (2.2 per cent) failed to respond to 
any of the 8 inoculations to which it was subjected. 

We have summarized our inoculations in which the initial one was 
either unfiltered or filtered serum. 

Five monkeys received a first inoculation of virulent unfiltered 
serum ; three of the five animals failed to respond to this inoculation. 
Of these three, two responded promptly to the first immunity test 
(second virulent inoculation), while one, rhesus No. 221, has so far 
resisted five successive immunity tests (6 virulent inoculations). 

Seven monkeys received a primary inoculation of filtered serum; 
none of the seven responded to this initial inoculation. When sub- 
jected to an immunity test, however, all but two (Nos. 115a and 194) 
responded; in other words, two of the seven failed to react to the 
first injection of virulent material. One of these two (No. 194) re- 
sponded to the second immunity test and the other (No. 115a) to the 

If now we combine the results summarized in the foregoing, we 
find that of 58 animals, 13, or 22.5 per cent, failed to react (i. e., did 
not become infected) after one injection of virulent blood or blood 
serum; 5, or 8.6 per cent, failed to react after two injections; and 
2, or 3.5 per cent, after three injections. 

It is evident that a very large proportion (22.5 per cent) of 
monkeys possess at least a transient immunity, and it seems reason- 
able to consider that in about 3.5 per cent of animals the resistance 
noted amounts to a permanent immunity. 

It may, perhaps, be objected that this is only an apparent im- 
munity, that the resistance is simply due to a virus of low or vary- 
ing virulence, to the smallness of the dose employed, the site of inocu- 
lation, or to the size or age of the animal. 


It is readily conceivable that different strains of virus may differ 
markedly in virulence. Analogies readily suggest themselves, and 
the results of our inoculations with virus from human sources ap- 
pear to furnish some experimental support for such a view. A 
summary of our inoculations with blood from human cases of typhus 
shows that only a small proportion, whether New York or Mexican 
cases, were successful. 

While, as we say, it is not improbable that in these cases viruses 
of differing virulence may have entered as an element, we do not 
believe that this factor enters into the results of the series of inocu- 
lations above considered ; for the inoculations in question were made 
with a single strain which we have successfully propagated through 
some 23 monkey generations, throughout which the virus, so far as we 
are able to discern, has maintained its original degree of virulence. 
The suggestion that age may enter as a factor in susceptibility has 
been advanced because it is held by some that children are less 
susceptible than adults. As a matter of fact, there is no good evi- 
dence to show that children are less susceptible to typhus than adults. 
It is probably true that the manifestations of typhus in a child are 
not in all respects like those in the adult ; that is, they are not typical, 
but this manifestly can not be regarded as indicating a difference 
in the degree of susceptibility. That this and the other objections 
cited are not valid may be clearly inferred from the fact, first, that 
of two monkeys of substantially the same size and vigor, both inocu- 
lated at the same time by the same route but with different quantities 
of the same virus, the animal receiving the larger dose (by 50 per 
cent) has failed to react; and, second, as has already been noted 
above, an animal may react after the second or the third inoculation, 
although the dose may be only half as large as that given in the 
immediately preceding ineffective inoculation. 

The existence of a more or less marked transient (or permanent) 
natural immunity is of great practical importance in all work on 
typhus. Great caution and conservatism must be observed in the 
interpretation of experimental results, especially negative results. 
We believe, too, that it may have a much broader significance and 
application. It will be recalled that Metchnikoff and Besredka, in 
their studies on antityphoid vaccination conclude that the ingestion 
of Bacillus paratyphoid-B may vaccinate against true typhoid. This 
conclusion is based on the observation that in one of two experiments 
a chimpanzee that had previously been infected experimentally with 
paratyphoid-B was subsequently refractory to infection with ty- 
phoid. Now, while the results of future work may reinforce this 
conclusion, the thought readily suggests itself that an occasional 

Anderson an< 

>n and] 
ger. J 



chimpanzee may be met with that may be transiently or permanently 
resistant to infection with typhoid. Indeed, these authors them- 
selves, in a previous communication, report that they met with only 
one failure in 16 experiments to infect anthropoids. We believe, 
therefore, that their conclusion is to some extent at least, if not 
altogether, invalidated. 

In a discussion of the susceptibility of the monkey it is essential 
to have a clear understanding of what one is to consider as a typhus 
reaction in this animal. Following an inoculation with virulent 
material the monkey continues for a period varying from 5 to 24 
days as if nothing had happened. As may be seen from Table No. 1, 
in about 90 per cent of cases the incubation period varies between 
6 and 10 days. 

Table No. 1. 


Number of 









* 20 
















At the end of this period the temperature of the susceptible animal 
rises fairly rapidly as a rule, sometimes gradually or at times very 
abruptly. The fever reaches its fastigium in 36 to 48 or 72 hours; 
it then continues for a variable period of 1 or 2 to 5 or more days, 
then defervesces. The defervescence, like the invasion, is vari- 
able ; although usually gradual, it is frequently rapid or even critical. 
In brief, the course of the fever in the monkey is essentially like that 
of the fever in man. 

The fever may be accompanied by loss of appetite, thirst, a ruf- 
fling of the fur, and a drooping posture ; very commonly, however, 
even with a well-defined febrile reaction, the animal except for some 
slight listlessness shows hardly any outward manifestations. In 
other words, the fever is the only definite index of a reaction. As 
may be seen from Table No. 2, in about 76 per cent of the cases the 
fever varies in duration between 6 and 10 da vs. 



Table No. 2. 

Duration of 

Number of 


































At the termination of the fever there is almost always manifest 
some degree of emaciation. Occasionally after the temperature has 
been normal for three or four days or a week it may go up a second 
time ; such a relapse may last 5 or 7 or more days and end in recovery 
or death. We have met with febrile recrudescence or relapse in 4 
of 103 cases. 

Although in appearance a mild disease, we have thus far had 4 
deaths in a total of 103 cases of typhus in the monkey. This total 
of cases includes 10 induced with the Mexican virus. Segregating 
these, we have four deaths in 93 cases of the disease induced with 
the New York strain (Brill's disease), a mortality notably higher 
than that reported by Brill in the human subject. 

An animal that has presented a reaction such as above described 
is immune from subsequent infection. In Table No. 3 we present the 
results of immunity tests in monkeys that had presented typical pri- 
mary reactions. It will be seen that in no instance has such an 
animal responded to a subsequent immunity test. Such an immunity 
may last a long time, as is shown by the following: Adela, a female 
rhesus, was originally infected by an intraperitoneal injection of 6 c.c. 
of defibrinated blood from a patient with (Mexican) typhus on Jan- 
uary 11, 1910. This animal developed a marked typhus, terminating 
on January 29-30, 1910. Between November 9, 1911, and March 0, 
1912, this monkey was given four inoculations of typhus blood, all 
of which it resisted absolutely, showing that it was still immune after 
at least two years. 

Anderson and] 



Monkey No. 


Co. in- 




/Nov. 23,1911 
\Dcc. 8,1911 
/Dec. 30,1911 
1 J an. 1, 1912 
/Nov. 23,1911 
\Dec. 8,1911 
(Nov. 29,1911 
{Dec. 12,1911 
[Jan. 11,1912 
[Nov. 9,1911 

IDec. 2,1911 

iDec. 22,1911 

Mar. 30,1912 

Mar. 30,1912 

(Dec. 29,1911 

{ Jan. 1,1912 

[Feb. 1,1912 

Feb. 1,1912 

/Feb. 1,1912 

\Feb. 23,1912 

Jan. 10,1912 

Jan. 10,1912 

(Nov. 9,1911 

IDec. 2,1911 

(Jan. 10,1912 

iMar. 6, 1912 



Rhesus 306 


Rhesus 95 

Case 19M 

Case 38M 


Rhesus 127 

Case 39 M 


Rhesus 30(5 


Rhesus 133 

Case 19M IVrilrmoiim 

Rhesus 170 


Rhesus 142 

Rhesus 161 



Rhesus 186 


Case 1M 

Vein and subcutane- 


Rhesus 158 

Case KIM 

Case 26M 


Rhesus 188 

Rhesus 234 


Rhesus 210 

Rhesus 234 


Case 35M 


Rhesus 306 

Case 39M 


Rhesus 184 


Rhesus 315 

Rhesus 184 


Rhesus 184. 


Rhesus 316 

Rhesus 200, 203,204... 
Rhesus 187.. 

Rhesus 317 


Rhesus 318 

Rhesus 187. 


Case 1M 


Case 16M 


Rhesus 500 

Rhesus 187 


Rhesus 213, 312 


Ordinarily, therefore, a well-marked febrile reaction may be inter- 
preted as typhus without subjecting the animal to an immunity test. 
When, however, the fever is slight or its course atypical — that is, 
when we have what may be designated as an " abortive " fever — this 
can not be construed as a typhus reaction unless the immunity test 
proves the animal resistant to infection, and even then not without 
some reserve. Should the immunity test in such cases show that 
resistance has not been conferred, a diagnosis of previous typhus is 
not permissible. 

The experimental work of Anderson and Goldberger, Ricketts and 
Wilder, Gavino and Girard, and more particularly that of Nicolle 
and Conseil, has developed a solid basis for the conclusion that the 
virus of typhus is present in the blood at least throughout the febrile 
period. The latter two workers were the first to try to determine 
whether the virus is present in the blood, either before the beginning 
of the fever or at its defervescence. As the point has important 
bearings, we repeated their work, and as a result concluded (1) that 
satisfactory evidence has not yet been adduced that the blood of a 
monkey infected with typhus is virulent in the prefebrile stage, and 
(2) that the blood of the monkey may still be virulent 24 to 32 hours 
after the return of the temperature to normal. 

Recognition of the infectivity of the blood naturally leads to the 
search for the element or elements of the blood in which the virus 
is localized. Nicolle, Conor, and Conseil have argued in favor of 
an intraleucocytic localization of the virus, and believe that the red 
corpuscles, after- one washing, are no longer infective (or onty incon- 
stantly so) . We believe this to be an error of interpretation, due to 


a disregard of the possibility that the monkey is not at all times sus- 
ceptible to infection. In a single experiment to test this point we 
found that the corpuscles were infective after three washings. This 
would appear to suggest that the virus adheres very closely to the 
blood cells. We believe, however, that the real explanation is to be 
found, at least in large part, in the inherent defect of the method 
(centrifugation) employed for the separation of the virus and the 
corpuscles. Just as a considerable number of leucocytes are entan- 
gled and carried down by the red blood cells in centrifuged blood, so 
we believe the virus is carried down by the precipitated cells. 

The question of the filterability of the virus, as it exists in the 
blood, has been the subject of considerable research, but the results 
recorded do not appear to be altogether harmonious. After a care- 
ful consideration of the experiments reported by others and the 
results of our own experiments we are of the opinion that there is 
no evidence to show that the virus in the blood of typhus is able to 
pass the Berkefeld filter and, incidentally, that virulent typhus blood 
contains no toxin or contains it in quantities too small to cause an 
appreciable increase in the normal resistance of the monkey when 
injected even repeatedly in the ordinary doses. 

The virus in the blood is not very highly resistant. We have 
found that drying for 24 hours and heating to 55° C. for 5 minutes 
deprives it of infectivity. It may resist freezing, however, for at 
least 8 days. Gavifio and Girard report that the infectivity of the 
blood is lost after an hour's contact with phenol in 0.5 per cent solu- 
tion, but that it is retained after an hour's contact with saponin in a 
solution of like strength. 

Notwithstanding that the transmission of typhus fever by the 
body louse has been shown by Nicolle and his coworkers, by Ricketts 
and Wilder, and by ourselves, and also that the disease may perhaps 
be transmitted by the head louse, there are nevertheless those who 
believe that there may be other methods of transmission, especially 
by the expired air or buccal secretions. 

In experiments conducted by ourselves in regard to this point we 
concluded that the buccal secretions are not infective for the monkey 
and that therefore droplet infection plays no part in the transmission 
of the disease. This is in distinct contrast with the method by which 
measles is spread, as we have shown that in that disease the virus is 
contained in the buccal and nasal secretions collected before and 
within 48 hours after the first appearance of the eruption. 

Anderson, John F., and Goldberger, Joseph : On the etiology of tabardillo or 
Mexican typhus. An experimental investigation. Jonrn. Med. Research, vol. 
22. Jwne, 1910, p. 400-481. 

& : The period of the infectivity of the blood in measles. 

Journ. Am. Med. Assn., July 8, 1911, p. 113. 

GSl d d e be S r?er? nd ] IMMUNITY TO TYPHUS. 25 


Dorset, M. t McBryde, and Niles: Further experiments concerning the pro- 
duction of immunity from hog cholera. Bulletin 102, Bur. Animal Industry, 
U. S. Dept. Agriculture, Washington, 1908. 

Dreyer, W. : Untersuchungen iiber den Typhus exanthematicus in Agypten. 
Arch. f. Schiffs- u. Tropen-Hygiene. Leipzig, May, 1911, vol. 15, p. 319-325. 

Gavino and Girard : Cuarta nota sobre el tifo experimental en los monos 
inferiores. Publicaciones del Inst. Bacteriol6gico Nacional, Mexico, November 
9, 1910. 

Marks, H. K. : Infection of rabbits with the virus of poliomyelitis. Journ. 
Experimental Med., vol. 14, 1911. 

McCoy, George W. ; & Chapin, Charles W. : Immunity of wild rats (Mus 
norvegicus) to plague infection. Public Health Bulletin No. 53, U. S. P. H. & 
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Metchnikoff, E. ; & Besredka, A. : Recherches sur la fievre typhoide experi- 
mentale. Ann. de Tlnstitut Pasteur, Paris, March, 1911, p. 192-221. 

& : Des vaccinations antityphique*. Ann. de Tlnstitut Pasteur, 

Paris, December, 1911, p. 865-881. 

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September, 1910. 

& : Le typhus experimental du singe especes sensibles, passage, 

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de Tlnstitut Pasteur, Paris, January, 1911, vol. 25, p. 13-55. 

, Conor; & Conseil: Propri§tes du virus exanthematique. Ann. de 

Tlnstitut Pasteur, February, 1911, p. 97-119. 

; & Conseil : Reproduction experimentale de la rougeole chez le bonnet 

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, Conseil; & Conor: Le typhus experimental du cobaye. Ann, de 

Tlnstitut Pasteur, Paris, April 25, 1912, p. 250-263. 

; & Conseil: Experiences concernant TimmunitS. Idem, p. 275-280. 

& : Animaux refractaires. Idem, May 25, 1912, p. 232-234. 

& : Essais de traitement. Idem, p. 334-348. 

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etiologla y seroterapia del tabardillo. Dictamen de la Comisitfn." Gaceta 
M6dica de Mexico, Apendice, Mexico, 1908. 

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Wilder, Russell M. : The problem of transmission in typhus fever. Journ. 
Infectious Diseases, Chicago, July 19, 1911, p. 101. 




Peyton Rous, M. D., and James B. Murphy, M. D. 

[From the laboratories of the Rockefeller Institute for Medical Research.] 

The present paper has to do with a sarcoma of the chicken, 1 which 
has been transplanted from one to another of 32 series of fowls, and 
in this manner has been kept growing in our laboratory for a period 
of nearly three years. The chief interest of the disease lies not in 
the illustration it affords of the behavior of transplantable tumors in 
the bird — a subject of which very little has been known — but in the 
fact that the growth's cause has been found in a filterable agent, 1 , 2 
almost beyond doubt a living organism. The presumption would 
naturally be that a growth so caused is a granuloma, not a tumor; 
and for that reason the characters of the disease have been subjected 
to especially careful scrutiny. 

The original or " spontaneous " growth was found in the subcuta- 
neous tissue of a young hen and was transplanted while the host was 
yet alive. Histologically it was a spindle-celled sarcoma, in some 
parts myxomatous, in others containing giant cells of sarcomatous 
type, as distinct from those seen in the granulomata of the fowl, or 
about foreign bodies. The transplantation of the fresh tissue to 
other chickens was successful, and the growth was thus established for 
experimental purposes. In the course of repeated transmission, its 
malignancy has been much enhanced. Of the many hundred deriva- 
tive growths, most have had the structure of a spindle-celled sarcoma. 
They have been made up of large, more or less attenuated, spindle 
cells coursing in irregular strands and supported by a scanty, vas- 
cular framework. The remaining growths have shown striking 
variations within the type, suggesting those which have been noted 
from time to time (Bashford, Lewin) in the transmissible malignant 
tumors of mammals. For example^ the sarcoma is occasionally 
formed of oat-shaped or bluntly fusiform cells, or of cells almost 
spherical; or many giant cells may be scattered through the tissue; 
or there may be a mixture of all the cells mentioned, resulting in a 
strikingly polymorphous appearance. Only of late have such varia- 
tions been prominent. 3 All the growths, histologically considered, 
are tumors. They can not be confused with the ordinary granu- 
lomata or with the tissue of chronic inflammation. 

Microscopically, the growth which arises after a routine implan- 
tation of the sarcomatous tissue in a fowl's pectoral muscles is a dis- 
crete elastic mass, lenticular, spherical or ellipsoidal, which as a 
rule enlarges rapidly and soon projects more or less sharply from 
the body contour. In hosts somewhat resistant, it is especially well 


defined and is often encapulated. In them it is prone to myxomatous 
change, being then semigelatinous. Id other partially resistant hosts, 
it is hard and fibrous, finely striated on section, and grayish-yellow. 
In very susceptible fowls it invades diffusely, and is grayish-pink, 
homogeneous, and gristly, or more often friable. In the latter case 
especially it is liable to soft, central necrosis, and to extensive hemor- 
rhages into its substance with cyst formation. 

The rapidity with which the sarcoma sometimes grows is very 
remarkable, though, all things considered, it is not more so than in 
the case of certain mammalian tumors, notably a mouse sarcoma 
described by Ehrlich. Within three weeks after the implantation of 
a tissue graft less than 2 millimeters in diameter there may develop 
from it a mass 12 by 6 by 6 centimeters. Over 40 per cent of the cells 
in the more active portions of such a growth may be in process of 
division at one time. 4 Amitosis is much more frequent than mitosis. 

The sarcoma's increase in size is usually accompanied by an in- 
vasion and replacement of normal structures. This may be beautifully 
seen when the growth lies in striated muscle. The neoplastic cells 
frequently penetrate into the individual fibers and here, multiplying 
and eroding, they replace the muscle substance in toto, though the 
outline of the fiber is retained. Frequently the blood and lymph ves- 
sels are entered, resulting in metastases. Over half the fowls now 
dying of the growth have secondary nodules in the viscera. Usually 
the distribution is by the blood stream, as with other sarcomata ; and 
the lungs are affected first, later, the organs supplied by the greater 
circulation. The lungs are sometimes nearly replaced by coalescing 
nodules, and may be doubled in bulk. Metastases are frequent in the 
liver, heart, and ovary, and are met less often in kidney, spleen, giz- 
zard, and bone marrow. A widespread dissemination may occur on 
the surface of the peritoneal cavity. 

The host at first seems unaffected by the developing growth, but 
soon it begins to lose weight, becomes anemic and emaciated, and, in 
the absence of intercurrent processes, dies in coma. 

These are the superficial characters of a tumor, yet in themselves 
they do not suffice to identify the growth as one. The essential fea- 
ture of tumors, which distinguishes them from other new formations 
of tissue, has yet to be considered, namely, that of growth by division 
of the cells already neoplastic, as contrasted w T ith growth by a patho- 
logical change in cells previously normal. Are the extension and dis- 
tribution of the chicken sarcoma referable to this cause? 

The problem has been studied in several ways. The direct histolog- 
ical evidence thus far collected would suffice to settle it in the case of 
any other growth. The histological character of the growth, the 
number of division figures, the evidence of pressure on surrounding 


structures, the noteworthy invasion and replacement by a tissue 
which is often very distinct from that of the structure attacked, the 
extension of strands of the growth into the lumen of blood vessels, 
the casting off of cell emboli, and the lodgment and growth of these 
emboli at distant sites, may all here be cited as indicating growth 
" aus sich heraus," to use Eibbert's words. We have repeatedly found 
all stages in the formation of metastases by means of cell emboli. 
But experimental evidence is more convincing. A suspension of the 
fresh tumor tissue was injected intravenously into a number of nor- 
mal fowls, and after some days these were killed, and the lungs ex- 
amined in serial section. It was found that the sarcomatous nodules 
developed from -tumor bits that had lodged in branches of the pul- 
monary artery and proliferated there, penetrating at length through 
the vessel coats into the pulmonary tissue. Many of the tumor emboli 
had failed to survive, and about these the sarcoma did not arise. By 
a study of the fate of numerous grafts of a single sarcoma implanted 
in a susceptible fowl, and removed at operation on successive days, 
it has been shown that the sarcomatous tissue survives transplanta- 
tion to other hosts, is vascularized, and by its proliferation gives rise 
to the new growth. In resistant fowls the implanted tissue dies and 
no sarcoma arises. 

It is certain then that the chicken sarcoma grows " aus sich heraus," 
possesses, in other words, that fundamental character by which at 
present we distinguish tumors. But it may well be asked, Does not 
the growth extend also by the infection of neighboring cells? Cer- 
tainly such a possibility can not be ruled out on histological evidence 
alone, any more than it can in the case of the mammalian sarcomata, 
and the demonstration of an agent causing the growth would appear 
a priori to render such infection very likely in its case. But we have 
found that a number of circumstances, later to be enumerated, limit 
the agent's activity, 5 and to such an extent that, even by specially 
devised experiments, we have been unable to show that infection of 
the sort mentioned has any share in the sarcoma's ordinary mani- 
festations. These are referable entirely to growth and dissemination 
M aus sich heraus." 

A further and interesting proof that the chicken sarcoma is a 
neoplasm is found in the behavior of the growth in the various hosts 
to which it has been transplanted. For some time workers have 
known that there are certain conditions affecting the success of tumor 
transplantation, which are either entirely different from those influ- 
encing the transmission of infectious diseases or are much more pre- 
cise in their effect. (L. Loeb, Schone, Bash ford, Fichera, Rous.) 
These conditions are largely the same ones that affect the transplanta- 
tion of normal tissues. The fact is one of the most significant that 


has resulted from modern cancer research, and has furnished a strong 
argument to those theorists who refer the cause of cancer to an in- 
trinsic cell derangement, as distinct from an infectious agent. But 
it happens that the chicken sarcoma, though indubitably caused by an 
extrinsic agent, is markedly influenced by the conditions mentioned. 

Prominent among such conditions is blood relationship, a factor 
which plays so large a part in the success of surgical grafting. Our 
original chicken sarcoma occurred in a fowl of pedigreed stock and 
was transplantable at first only to this fowl's immediate relatives 
(fowls in the relationship of half brother, half sister, uncle, and 
aunt). In nonrelated fowls of exactly the same breed (barred Plym- 
outh Rock) , it would not grow. Only after repeated transplantation, 
which resulted in enhanced malignancy, did it become less precise as 
regards a host. Even when last tested (eighth tumor generation), it 
grew best in chickens of the original strain. Despite repeated efforts 
it has never been successfully transferred to mammals, rabbits, guinea 
pigs, rats, mice), or to other birds than chickens (pigeons, ducks). 

The physical condition of the host has a marked influence on the 
chicken sarcoma, the reverse of that obtaining for the usual infectious 
diseases, and similar to that noted in the case of the transplantable 
mammalian tissues, normal and neoplastic. An emaciating illness, 
instead of predisposing the host, renders it relatively insusceptible, 
and may cause the rapid retrogression or even the temporary disap- 
pearance of well-developed sarcomata. 2 The growth is more easily 
transplanted to young hosts than to old, and grows more rapidly in 
them, a fact already known of the transplantable mammalian tissues. 
By inoculations into chick embryos (seventh to tenth day), without 
disturbing their development, we have found that embryos are espe- 
cially susceptible as hosts. 6 Some adult fowls exhibit a natural 
resistance that is independent of age, condition, or variety. Though 
apparently very suitable as hosts for the tumor, these fail to develop 
a growth even after repeated inoculations with active tumor tissue. 
In some chickens, too, the sarcoma, after growing for a while, retro- 
gresses without evident reason, leaving the host temporarily resistant. 
All the types of resistance mentioned have their parallel in mammals. 
The histological processes about the retrogressing tumor or the 
unsuccessful graft are essentially similar in the case of the chicken 
tumor and rat and mouse tumors. 5 

So much, then, for the characters of the chicken sarcoma. They 
stamp the growth as a tumor in all that the word implies at this 
day when our conception of the neoplastic process rests, not merely 
on clinical and anatomical data, but on broader experimental findings. 
So close a correspondence between the tumor phenomena in the bird 
and those in mammals could hardly have been expected. 


Our first attempts to determine the chicken sarcoma's cause were 
made without expectation that they would lead to positive results. 
By three methods, an etiological agent, as distinct from the tumor 
cells, has been demonstrated, viz, by filtration, by drying, and by 
glycerinization. 1 ' 2 > 7 The fluid obtained by passing an extract in 
Ringer's solution of the fresh sarcomatous tissue through a Berkefeld 
filter (N) will give rise to the tumor; sarcomatous tissue dried 
in vitro over sulphuric acid, ground to powder, and so kept for weeks 
or months, will likewise cause it ; and so will tissue kept for weeks in 
50 per cent glycerin. 8 No special complexity has attended our use 
of these procedures. The tumors engendered by filtrate, or by the 
dried or glycerinated tissue, do not differ from those resulting from 
transplantation, except that they take, as a rule, very much longer to 
appear and often grow much more slowly. They metastasize, and are 
capable of transplantation, forming the potential source of any 
number of growths from each of which the agent may be obtained 
in quantity. 

The characters of the agent are those which we associate with 
microorganisms ; 7 and it would appear to be among the larger of 
the filterable causes of disease, failing, as it does, to pass through a 
Chamberland bougie, though it goes easily through a Berkefeld cyl- 
inder (N or V) impermeable to Bacillus fluorescens liquefaciens. 
Our repeated attempts to observe the agent directly and to cultivate 
it in vitro have thus far failed. In dried or glycerinated tissue it 
undergoes a gradual attenuation. In fresh sarcomatous tissue it sur- 
vives repeated, rapid freezing and thawing, which reduces the tissue 
itself to a pulp. It is rendered inactive by heat (55° C. for 15 
minutes) a little greater than that which kills the associated tumor 
cells (50° C.), as shown by the results of attempts to grow them in 
vitro. It is quickly rendered inactive by autolysis, by chloroform 
and toluol, in the proportions used to prevent bacterial growth in 
autolytic preparations, by 2 per cent carbolic acid, and by 50 per cent 
alcohol. Like the animal organisms in distinction from most of the 
vegetable ones (v. Prowacek) it is destroyed by high dilutions of 
seponin and by bile. 

The relation of the agent to the disease which it causes is at present 
unique in pathology, for the behavior of the sarcoma is entirely 
referable, as already shown, to the cells composing it. Recent work 
has made evident some of the reasons for this. 

In the first place the agent elicits of itself no noteworthy immunity. 
The resist ni ice induced in fowls by retrogression of the sarcoma is 
very weak, is frequently transient, and its histological manifestation 
about n fresh graft of the sarcomatous tissue is of the sort which we 
have come to recognize as indicating resistance to the strange tissue 
as such. With the object of obtaining a more marked resistance 


many chickens have been injected with gradually increasing amounts 
of the dried sarcomatous (issue, attenuated at first by heat. Most of 
these have sooner or later developed the sarcoma and died of it. 
The sera of the fowls which survived and of rabbits which had been 
similarly injected have shown only very dubious powers of neutrali- 
zation when incubated in vitro with the agent. The absence of well- 
defined immunity processes directed against the agent as such ex- 
plains very well why immunity processes directed against the trans- 
planted tumor tissue as strange tissue, and present in any event, 
come to claim attention. Their existence in the case of this and other 
growths does not mean necessarily that an etiological agent other 
than the cells themselves must be absent. It means simply that the 
phenomena of resistance to such an agent, if present, are less well 
marked than those directed against the cells themselves. 

Secondly, the agent does not act upon normal connective tissue. 
To bring about a neoplastic change it must have opportunity to 
affect connective tissue in which a proliferative reaction is occurring. 
A large quantity of Berkefeld filtrate containing the agent in active 
form, when introduced through a fine needle into normal tissue has 
only rarely results in a growth, and this growth develops in the 
track of the injecting needle, but if to the filtrate there be added a 
little sterile Kieselguhr (which produces, as Podwyssozki has shown, 
a profuse connective tissue reaction) tumors follow a large per- 
centage of the inoculations, and they develop from numerous foci 
where the reaction to Kieselguhr is going on. • 

Third, the agent's action in producing tumor tissue by a change 
in cells not previously neoplastic is very sIoav as compared with the 
proliferation of these cells, once they have undergone a neoplastic 
change. The first few cells that become sarcomatous rapidly divide 
and elaborate the mass of tumor tissue. Their activity overshadows 
any coincident neoplastic transformation, granting, indeed, that the 
factor of cell derangement necessary for this be present. 

The existence of these three limitations to the agent's activity will 
largely account for the latter's failure to take an obvious part in the 
tumor's ordinary growth and distribution in the host. The existence 
of yet other limiting factors would explain why this failure is so 
nearly absolute. It is to such factors also, discovered and undis- 
covered, that the sarcoma's failure to appear as an epidemic disease, 
and its total lack of infectivity in the ordinary sense, must be at- 
tributed. During the last year Ave have collected some 30 spontaneous 
chicken tumors without encountering again the picture of the sar- 
coma ; and in our laboratory, during the last three years, there have 
been kept in close quarters large numbers of fowls with and without 
the disease, yet Ave have still to find an instance of its natural trans- 
mission under these circumstances. 


The results of the study thus briefly summarized offer more than 
a suggestion as regards the etiology of malignant tumors. They 
afford a rational explanation, founded on an actual instance, of some 
of the more puzzling features of these growths. The peculiarities 
of occurrence of malignant growths, the importance of tissue derange- 
ment in their etiology, their growth and dissemination by means of 
cells, their behavior on transplantation, are quite compatible with 
the assumption that they are caused by an agent limited in its action 
by conditions somewhat similar to, but doubtless more complex than, 
those influencing the agent causing the chicken tumor. But whether 
this assumption be correct, the work of the future must determine. 
Certainly the findings with the chicken sarcoma largely demolish 
the theoretical objections to an extrinsic cause for cancer. 

Note. — Since the above article was written we have demonstrated 
that a filterable agent is the cause of an osteo-chondro-sarcoma of 
the fowl, recently propagated in this laboratory. The agent causing 
this growth, like that of the spindle-celled sarcoma, requires for its 
action an associated cell derangement, but true cartilage is laid down 
in the growths to which it gives rise. 9 

1 Peyton Rous, Jour. Exp. Med. 1910, xii, 696. J. A. M. A. 1910, liv, 1805. 

2 Ibid., Jour. Am. Med. Ass. 1911, lvi, 198; Jour. Exp. Med. 1911, xiii, 397; 
Proceedings Am. Philosoph. Soc. 1912, li, 201. 

8 An article dealing with these variations will shortly appear in the Jour, 
of Exp. Med. 

4 J. B. Murphy and Peyton Rous, Jour. Exp. Med. 1912, xv, 119. 

5 Rous and Murphy, Jour. Exp. Med. 1912, XV, 270. 

Rous and Murphy, Journal of the American Medical Association, 1911, LVI, 
741; Journal of Experimental Medicine, 1912, XV, 119. 

7 Rous and Murphy, Jour, of Amer. Med. Assoc, 1912, LVIII, 1938. 

8 Two other methods, namely, freezing and thawing the fresh tumor tissue, 
and heating it at 50-53° C. allow a less satisfactory differentiation of the agent 
from the cells. 

9 See Peyton Rous, J. B. Murphy, and W. H. Tytler, Journal of the American 
Medical Association, 1912, LIX, 1793. 



By Prof. Adolf Dieudonn£, University of Munich, Germany. 

In der Deutschen amtlichen Anweisung fur den bakteriologischen 
Nachweis der Cholera ist bereits ein stark alkalischer 3 procentiger 
Agar empfohlen, auf dem die Entwicklung anderer Keime wesentlich 
eingeschrankt wird. Von diesem Nahrboden. dessen Elektivitat auf 
der starken Alkalitoleranz der Choleravibrionen basiert, ausgehend, 
hat Dieudonne durch Zusatz von bestimmten Mengen Rinderblutes, 
das speciell auf Vibrionen wachstumsfordernd einwirkt, einen 
neuen Choleraelektivnahrboden angegeben, durch den die bakteri- 
ologische Untersuchung auf Cholera wesentlich vereinfacht wird, 
und ihr Nachweis mit weit grosserer Sicherheit gelingt. Bei der 
Bereitung dieses Nahrsubstrates werden defibriniertes Rinderblut 
und Normalkalilauge zu gleichen Teilen gemischt and J Stunde im 
Dampfstoff sterilisiert ; die Mischung wird dann mit 3 procentigem, 
genau auf den Neutralpunkt eingestelltem Agar im Verhaltnis von 
3 : 7 versetzt, und das Ganze sof ort in Petrischalen ausgegossen. 
Dabei verwendet man nach dem Vorschlag von Neufeld u. Woithe 
am besten 15 ccm Nahrbodenmasse fiir je 1 Petrischale von 10 ccm 
Durchmesser. Wenn die Nahrbodenschicht festgeworden ist, werden 
die Schalen geschlossen und mit dem Deckel nach unten je nach dem 
Feuchtigkeitsgehalt 12-15 Stunden lang im Brutschrank bei 37° 
aufbewahrt. Es empfiehlt sich vorher zwischen Ober- und Unter- 
schale und ihre Wandungen kleine Streifen Fliesspapier einzulegen, 
sodass die Schalen teilweise off en sind und ein Ansaugen und Ent- 
weichen der Feuchtigkeit und der Abdampfstoffe (Ammoniak) 
erzielt wird. 

Der Dieudonne'sche Blutalkaliagar hat sich bei den schr zahl- 
reichen Nachpriifungen und in der Praxis bei Choleraepidemien 
bereits ausgezeichnet bewahrt. Allerdings haftet ihm der Nachteil 
an, dass er nicht sofort, sondern erst nach einiger Zeit, im ungiin- 
stigsten Fall erst etwa 18 Stunden nach dem Ausgiessen der Platten, 
benutzt werden kann, weil bei sofortiger Verwendung jedes Bak- 
66692— vol 2, pt 1—13 3 33 


terienwachstum. auch die Entwicklung der Choleravibrionen unter- 
driickt wird. Um diesen Missstand abzuhelfen, sind von verschie- 
denen Autoren eine Anzahl Modifikationen angegeben worden, von 
denen die bekanntesten, namlich die von Neufeld-Woithe, Esch, 
Pilon, Hoffmann-Kutscher und Moldavan, im folgenden mitbe- 
sprochen werden solien. 

Neufeld u. Woithe suchten einen sofort verwendbaren Blutal- 
kaliagar dadurch zu gewinnen, dass sie unmittelbar vor dem Giessen 
der Platten auf je 100 ccm des Nahrbodens 2 ccm 10 procent. 
Milchsaure zusetzten behufs Bindung des Ammoniaks, bezw. zur 
Neutralisation eines etwaigen Ueberschusses der nach dem langen 
Kochen etwa noch iibermassig vorhandenen Lauge. Dieser Nahr- 
boden, der nach J stundigem Troclnien der Platten im Brutschrank 
von 60° sofort benutzt werden kann, behalt aber seine Elektivitat 
fiir Cholera nur kurze Zeit, da nach 24-48 Stunden die Alkalescenz 
infolge der zunehmenden, durch den Zusatzt der Saure eintretenden 
Neutralisation stark herabgesetzt wird. 

Esch benutzte bei Herstellung seiner Modifikation 5 g kiiufliches 
Hamoglobin (von der Firma Marck in Darmstadt), das er in 15 
ccm Normalnatronlauge +15 ccm Aqua destillata aufloste. Das 
Gemisch wurde 1 Stunde in Dampf sterilisiert, und davon wurden 
15 ccm mit 85 ccm lackmusneutralen 3 procentigem Agar vermengt 
und zu Platten gegossen. Nach kurzer Trocknung bei Zimmertem- 
peratur konnen die angelegten Platten bereits verwendet werden. 
Allerdings bemerkt der Autor selbst, dass die Elektivitat seines 
Ersatznahrbodens nicht den gleich hohen Grad wie der Originalagar 

Pilon vertritt die Auffassung, dass die anfangliche totale Wacha- 
tumshemmung des Dieudonne'schen Blutalkaliagars nicht, wie 
Huntemuller annimmt. auf der Ammoniakentwicklung beruhe, 
sondern dass durch den urspriinglich hohen Alkalilaugengehalt des 
Nahrsubstrates die Entwicklung der Choleravibrionen unterdriickt 
werde. Erst wenn also die Alkalilauge durch die Kohlensaure der 
Luft in Karbonat umgewandelt worden sei, konne man die Original- 
blutagarplatten benutzen. Er suchte daher einen sofort gebrauchs- 
fahigen Nahrboden dadurch zu erzielen, dass er die Kalilauge durch 
Sodalosung ersetzte. Nach seinen Angaben werden defibriniertes 
Blut, am besten Schweineblut und 12 procent Sodalosung zu gleichen 
Teilen gemischt und nach 1 stiindiger Sterilisierung im Dampftopf 
mit lackmusneutralem 4 procentigem Agar im Verhaltnis 3:7 ge- 
mengt. Die frisch gegossenen festgewdrdenen Platten bediirfen dann 
vor dem Gebrauch noch einer ] stiindigen Trocknung im Brutschrank. 

Einen weiteren Ersatz fiir den Originalagar stellt der von Hoff- 
mann und Kutscher angegebene, getrocknete Dieudonne'-Blutalka- 
liagar. Er wird in der AVeise gewonnen, dass man den gewohnlichen 


Dieudonne'schen Originalniihrboden in Petrischalen ausgiesst und 
im Faust-Heim'schen Apparat trocknet. Man erhalt so ein braunes, 
ziemlich grobkorniges Pulver, das, vor Feuchtigkeit geschiitzt, lange 
haltbar ist.. Zur Bereitung des gebrauchsfertigen Nahrbodens lost 
man 8 g dieses Pulvers in 100 ccm Wasser auf und kocht das Gemisch 
\ Stunde im Dampftopf. Vor dem Giessen der Platten empfiehlt 
es sich, den Nahrboden kurze Zeit noch im Kolben stehen zu lassen, 
weil sich die truben Bestandteile dann am Boden absetzen, und das 
Nahrsubstrat ziemlich hell und durchscheinend wird. Die frisch 
gegossenen, abgekuhlten Platten sind ebenfalls nach kurzer Trock- 
nung im Brutschrank bei 60° verwendbar. 

Moldavan mischt Blutalkali und Agar im Verhaltniss von 1 : 4. 
Die gegossenen Platten bleiben 6 Stunden (also fur die Anreicherung 
in Peptonwasser) unbeniitzt bei Zimmertemperatur stehen. Nach 
dieser Zeit beimpft erweisen sie sich zwar schon etwas weniger elek- 
tiv als de*r Originalniihrboden, aber giinstiger fiir das Wachstum der 
Cholera vibrionen, sodass-letztere wenn uberhaupt wachstumfahig, 
stets angehen. 

Aus diesen Ausfuhrungen geht hervor, dass die Herstellung dieser 
verschiedenen Nahrmedien sich bei samtlichen Substraten in 
derselben einfachen Weise durchfuhren lasst. Einen gewissen Vor- 
teil diirfte die von Esch angegebene Modification insofern bieten, 
als das von ihm benutzte Hamoglobin stets vorratig gehalten werden 
kann und die Aufbewahrung gut vertragt. Was das Aussehen der 
einzelnen Nahrbodenplatten betrifft, so zeigen die des Originalagars, 
der Neufeld-Woithe'schen und der Pilon'schen Modification eine 
dunkelbraune Farbe und sind undurchsichtig ; die Platten des 
getrockneten Blutalkaliagars, sowie die nach Moldavan und nach 
Esch hergestellten dagegen sind hell und ziemlich gut durchscheinend. 
Eine wesentliche Aufhellung auch der obigen 3 Nahrmedien erzielten 
Haendel u. Baerthlein, auf deren umfangreiche, im Kaiserlichen 
Gesundheitsamt durchgefuhrte Nachpriifungen sich unsere kritische 
Wertung des Originalagars und seiner Modifikationen im Wesent- 
lichen stiitzt, durch Verwendung alteren, defibrinierten Blutes, das 
einige Zeit im Eisschrank aufbewahrt worden war. Bei samtlichen 
Nahrboden mit Ausnahme der Neufeld-Woithe'schen Modification 
blieb die Elektivitiit fiir Cholera bei Aufbewahrung im Eisschrank 
lange Zeit gut erhalten. Dagegen erscheint eine langere Aufbe- 
wahrung des Blutalkaliagars im Kolben wenig angezeigt, weil durch 
das notwendige, wiederholte Kochen die Nahrboden rasch weich 
und briichig werden. 

Was nun das Wachstum der Cholera auf den erwahnten Nahrsub- 
straten betrifft, so entwickeln im Allgemeinen auf samtlichen 
Nahrboden altere wie frisch isolierte Kulturen ziemlich grosse, flache, 
rauchbraune, bezw. auf dem Esch'schen Blutagar graubraune Ko- 


lonien, die auf den Pilon'schen Platten am iippigsten wachsen. Einen 
gewissen Nachteil zeigt indessen der mit Milchsaurezusatz hergestellte, 
sowie der nach Moldavan gewonnene, indem trotz genauer vorschrifts- 
massiger Herstellung in einzelnen Fallen auch das Wachstum echter 
Cholera unterdriickt wird. Die Agglutinabilitat der Choleravibrio- 
nen, die nach der Angabe einzelner Untersucher bei dem Wachs- 
tum auf den blutnahrboden vermindert sein soil, ist wohl etwas 
verzogert wegen der Klebrigkeit des Materials, aber nicht in dem 
Masse, dass dadurch die Diagnosestellung leidet. Die chloleraahn- 
lichen Vibrionen wachsen auf dem Esch'schen und dem Pilon'schen 
Nahrboden ebenso gut wie echte Cholera, wahrend sie auf dem 
Dieudonne'schen Originalagar sparlicher gedeihen, auf den anderen 
Modifikationen verschiedentlich iiberhaupt nicht zur Entwicklung 

Nach den vergleichenden Untersuchungen von Haendel u. Baerth- 
lein iiber die entwicklungshemmende Eigenschaften der Nahrboden 
anderen, insbesondere Stuhlbakterien gageniiber ergaben sich 
zwischen den einzelnen Nahrsubstraten doch recht betrachtliche 
Unterschiede. Wenn man die verschiedenartigen Kokken in Abrech- 
nung bringt die zwar auf alien Nahrboden ziemlich haufig, wenn 
auch sparlich zur Entwicklung kommen, aber durch das Aussehen 
ihrer ausserst feinen Kolonien sich leicht von echter Cholera unter- 
scheiden lassen, also ohne praktische Bedeutung sind, so blieben die 
mit den Faces darmkranker itmd gesunder Menschen beimpften 
Platten beim Dieudonne'-Agar in 50— 60i procent, beim Neufeld- 
Woithe-Agar in 87 procent, beim getrockneten Dieudonne'-Agar in 
42 procent, beim Esch-Agar in 5, 7 procent, beim Pilon-Agar in 22 
procent und endlich bei der Moldavan-Modifikation in 65 procent der 
Falle steril. Wir sehen also, dass hinsichtlich der Elektivitat die 
Neufeld-Woithe'sche Modification an 1., der Dieudonne'sche Origi- 
nalagar und der nach Moldavan an 2., der getrocknete Dieudonne'sche 
Nahrboden an 3. Stelle stehen, wahrend bei der Pilon'schen und 
Esch'schen Modification die Verhaltnisse weniger giinstig liegen. 
Die innerhalb 24 h zur Entwicklung gekommenen Bakterien sind auf 
dem Nahrboden nach Neufeld-Woithe nur Vibrionen und Alkalige- 
nesstamme; auf dem Originalagar, dem getrockneten Agar und den 
Modifikationen nach Moldavan, Pilon und Esch wachsen ausser 
chosen Bakterienarten noch dem Protens und der Coligruppe zuzu- 
reehnende Kulturen, wobei auf dem Esch- und dem Pilon-Nahrboden 
speziell die Coli-Bakterien reichlich vertreten sind und zu Ver- 
wechselung mit Cholerakolonien fiihren konnen. Mittels des Pilon'- 
schen Nahrsubstrates wurden noch vereinzelt Paratyphus-Stamme 

Die Priifung der verschiedenen Nahrboden durch Aussaat aus 
Stiihlen, denen neben anderen Bakterien jeweils auch Cholera vi- 


brionen in fallenden Menge zugesetzt waren, zeigte, dass auf samt- 
lichen Blutalkalinahrboden im Allgemeinen wiihrend der ersten 24 
Stunden die Choleravibrionen entweder die anderen Bakterienarten 
glatt iiberwuchern, oder doch so weit zur Entwicklung kommen, dass 
ihre weitere Isolierung mit Hilfe von Agarplatten gut gelingt. Von 
praktisch wichtiger Bedeutung hinsichtlich der Abkiirzung der Chole- 
radiagnose ist dabei die Feststellung, dass sich haufig bei entspre- 
chend reichlichem Cholerawachstum von den .ersten Stuhlplatten 
schon die quantitative Agglutination und in manchen Fallen auch der 
Pf eiffer'sche * Versuch ausfiihren lassen. Bei sparlicher Entwicklung 
der Cholerakolonien oder gleichzeitigem, reichlichem Wachstum von 
choleraahnlichen Vibrionen oder Alkaligenes, bezw. Proteus auf den 
Platten, wie dies in der Praxis verschiedentlich vorkommen diirfte, 
empfiehlt es sich aber dringend, erst mit frisch angelegten Agar- 
kulturen die betreffenden Reaktionen vorzunehmen. Erwahnt sei 
auch, dass, was fiir die Weiterziichtung der isolierten Stamme von 
Bedeutung ist, auf dem Blutalkaliagar in der Regel keine Reinkul- 
turen von Cholera bei der Ziic^tung aus dem Stuhl sich entwickeln, 
wie man auf den ersten Blick haufig glauben konnte ; denn die iibri- 
gen Stuhlbakterien kommen zwar nicht zur Entwicklung, sie werden 
aber auch nicht abgetotet und konnen bei Abimpfung selbst von 
einer isolierten Cholerakolonie auf andere Nahrboden nach langerem 
Stehen der neuen Nahrsubstrate leicht zu schwerer Verunreinigung 
und Schadigung der betreffenden Cholerakultur fuhren. 

Zusammenfassend ergibt sich also, dass die verschiedenen Blut- 
alkaliagar-Nahrboden den bisher in der Choleradiagnose gebrauch- 
lichen Niihrsubstraten wesentlich iiberlegen sind. Durch ihre Benut- 
zung vereinfacht sich die Isolierung der Vibrionen aus verdachtigem 
Material ganz bedeutend und die Choleradiagnose lasst sich in den 
meisten Fallen nach kiirzerer Zeit stellen wie bisher. Unter den 
angegebenen Elektivnahrboden hat sich der Dieudonne'sche Original- 
agar am zuverliissigsten und besten bewahrt. 1 Zu beriicksichtigen 
ist allerdings, dass er nicht sofort, sondern erst etwa 18 Stunden nach 
dem Giessen der Platten gebrauchsfahig ist. 

Den ersten, verdachtigen Fallen Bis Firrdman zunachst eine der 
erwahnten Modifikationen benutzen, unter denen der getrocknete 
Dieudonne'sche Originalagar, oder die Modifikation nach Esch und 
Pilon als geeignet erscheinen, wiihrend die Niihrboden nach Neufeld- 
Woithe und nach Moldavan nicht die gleich grosse Sicherheit bieten, 
da sie wegen ihrer hohen Elektivitiit in seltenen Fallen auch auf die 
Entwicklung der Choleravibrionen zu stark hemmend einwirken. 
Fiir die Untersuchung der weiteren Falle ware indessen der Dieu- 
donne'sche Originalnahrboden angezeigt. 

Zum Schluss sei noch in Kurze auf zwei von Ottolenghi, bezw. vca 
Kraus angegebene Methoden eingegangen, welche einen Ersatz des 


Anreicherungverfahrens von Choleravibrionen in Peptonwasser 
bringen sollen. Nach den Angaben von Ottolenghi wird frische 
Ochsengalle durch Papierfilter filtriert, imd das Filtrat mit 3 ccm 
einer 10 procentigcn Losung von kristallisiertem Natriumkarbonat, 
so wie mit 0., 1 Kaliumnitrat versetzt. In die einzelnen Reagens- 
rohrchen werden dann je 5 ccm der Mischung abgefiillt und steri- 
lisiert. Gegeniiber dem Peptonwasser soil die Galleanreicherung 
auch bei sparlichem -Vorhandensein von Choleravibrionen im Stuhl 
noch gute Resultate zeitigen, ferner auf die verschiedenen Stuhlbak- 
terien und auch auf andere Keime stark entwicklungshemmend ein- 
wirken. Endlich gestattS dieses Verfahren die Verwendung ziemlich 
grosser Faces-Mengen. 

Kraus benutzt den schon von Dieudonne in seiner ersten Veroffent- 
lichung angegebenen fliissigen Blutalkalinahrboden. Je 100 ccm 
neutraler Bouillon werden mit 25 ccm Blutalkalilosung gemischt: 
Diese Blutalkalibouillon wird zuniichst 3 Stunden bei 50° und dann 
24 Stunden bei 37° gehalten, hierauf in Mengen von 5 ccm auf 
Reagensrohrchen aufgefullt und beimpft. Kraus bemerkt aus- 
driicklich, dass dieser Nahrboden unbeclingt durch einen Vorversuch 
auf seine elektiven Eigenschaften gepriift werden muss. Die fertige 
Losung ist langere Zeit hindurch haltbar. 

Mit der Gallenanreicherung von Ottolenghi erhalt man nach den 
Mitteilungen von Haendel und Baerthlein in manchen Fallen vielleicht 
etwas bessere Resultate als mit der Peptonwassermethode. Jedenfalls 
ist aber das Galleverfahren dem Peptonwasser nicht in dem Masse 
iiberlegen, dass sich seine ausschliessliche Einfuhrung an Stelle des 
Peptonwassers empfehlen wlirde. Wie bei der Peptonwasseranreiche- 
rung ist auch bei der Benutzung der Galle eine friihzeitige Unter- 
suchung nach etwa 4-6 Stunden erf orderlich. Die Methode von Kraus 
hat sich nach Haendel und Baerthlein in verschiedenen Fallen be- 
wahrt und gegeniiber dem Peptonwasserverfahren ganz wesentliche 
Vorteile gezeigt. Allerdings ist 5 wie ja Kraus selbst hervorhebt, bei 
der Herstellung jeder frischen Losung diese vor ihrer endgliltigen 
Verwendung auf ihre Elektivitat zu priifen. Nach Schiirmann und 
Abelin ist der Nahrboden fur die Choleradiagnose nicht brauchbar, 
da eine Anreichung der Choleravibrionen nicht beobachtet wurde. 

l Auch bei verschiedenen Epidemien, z. B. in Apulien, hat der Nahrboden gute 
Resultate ergeben und er scheint sich besonders auch zu Massenuntersuchungen 
zur Feststellung von Bazillentragern zu eignen. 


Dr. E. Libman, New York: Several years ago there was intro- 
duced by two of the assistants in the laboratory of the Mount Sinai 


Hospital, Drs. Bernstein and Epstein, a method by means of which 
it is possible to have always in hand blood ready for use in cultural 
work. The method is, in brief, the following : 

Blood is obtained at the slaughterhouse in flasks containing a 
certain amount of formalin and of ammonium oxalate. When this 
is received at the laboratory it is diluted with two parts of salt solu- 
tion. After standing in the ice box for 24 hours it is ready for use. 
One adds one-fifteenth (more may be used) volume of the blood to 
an}' medium. Bacteria of all kinds grow at least as well on these 
blood-media as on those prepared with fresh blood. 

The blood remains bright red for a varying length of time — after 
three or four weeks. We make a fresh supply every three weeks 
and are always ready for work requiring the use of blood in media. 


Dr. Charles Kkumwiede, Jr., Research Laboratory, Department of Health, New 

York, N. Y. 

In the preceding paper Dr. Dieudonne has given a detailed account 
of his medium and the various modifications which have been sug- 

During the summer of 1911 we used the original Dieudonne 
medium extensively. Where examinations were being constantly 
made, it seemed ideal. Where, however, examinations were infre- 
quent, it was unhandy because of the difficulties in its preparation. 
The necessity of waiting overnight before the plates could be used 
was removed in Pilon's modification. The necessity of obtaining 
blood as a basis for the medium still remained. This may be very 
inconvenient to obtain. For this reason we substituted eggs as a basis 
for the medium. The resulting medium is made as follows : 

A. Whole egg and water a. a., sodium carbonate cryst. 12 per cent. Mix in 

equal parts; steam in Arnold sterilizer for 20 minutes. 

B. Meat-free agar, viz, peptone, 1 per cent ; salt, $ per cent ; agar, 3 per cent. 

Mix A, 30 parts and B, 70 parts, while the agar is boiling hot. 
Pour medium thick plates, allow them to stand open for 20 to 30 
minutes to dry, and inoculate by surface streaking. 

In making the egg mixture the egg and water should be thoroughly 
shaken, the alkali added, and again thoroughly shaken. The thicker 
parts of the egg may be removed by filtration through a thin layer 
of cotton. The agar requires no change of reaction, and need not 
be filtered more carefully than to remove the coarser particles. 

On this medium the cholera colonies are distinctive. Examined by 
transmitted light, they have the appearance of being deep in the agar, 


and have a peculiar hazy, far-away appearance, due to an indefinite 
halo about the colony. When growth is more vigorous, viz, on longer 
incubation, this halo becomes surrounded by a zone of clearing. In 
practice, fishing from this type of colony has yielded cholera, and 
from this type alone. The only exception is in the case of cholera- 
like vibrios whose colonies are identical. Comparing this medium 
with the Dieudonne medium, the latter is somewhat more selective. 
This is more than offset by the fact that if growth of fecal bacteria 
should occur on the egg medium, the presence of even one cholera 
colony is immediately evident because of its distinctive characteristics. 

The various blood media are not completely selective, nor does the 
cholera colony on any we have tried approach in distinctiveness the 
colony as found on the egg medium. 

The advantages of the medium are the prompt availability of the 
ingredients, the ease of preparation, and the distinctiveness of the 
cholera colonies. For infrequent examinations, the first two are of 
great importance. As a routine medium it is economical. Ten eggs 
are sufficient for over 300 plates. 


Dr. A. J. Bendick, College of Physicians and Surgeons, Columbia University, 

New York City. 

Media containing lactose with litmus as an indicator for acidity 
have been extensively used for growing the colon bacillus and dif- 
ferentiating it from closely allied organisms. This type of medium 
is well exemplified in Wurtz's lactose litumus-agar, which consists of 
a 1 per cent lactose-agar colored with litmus. These media have sev- 
eral defects, chiefly due to the rapid diffusion of the acid, causing a 
general reddening of the adjacent medium. This necessitates having 
plates with few colonies and examining and counting while the colo- 
nies are still small. Also gas formation often occurs, ruining the 

To overcome these disadvantages, media consisting of stiffer agar 
have been devised, on which surface smears are made. This is the 
type of the Conradi-Drigalski medium, which consists of a special 
nutrient 3 per cent agar, to which crystal violet is added as an inhibi- 
tor for less resistant organisms than the typhoid bacillus. 

With the intention of limiting the diffusion of the acid formed 
by the splitting of the lactose I began to experiment by adding various 
alkalies to the medium. But such alkalies as NaOH and Na 2 C0 8 , 
when added in sufficient quantities, had a deleterious effect on many 


of the organisms, and, besides, colored the medium an intense blue, 
r which completely masked the production of alkalies, which produc- 
tion is of value in identifying typhoid colonies and those of the 
organisms of putrefaction. 

A neutral agar was desired in which the acid produced by the fer- 
mentation of the sugar would be neutralized in order to prevent its 
diffusion. This result can best be obtained by using an insoluble 
alkali or alkaline salt. 

The simplest and most efficient of the insoluble alkalies seems to be 
calcium carbonate — precipitated chalk. Being an impalpable pow- 
der, it is readily distributed through the medium, it exerts no inhibi- 
tion on the organisms, is readily obtainable everywhere, and is inex- 
pensive. Furthermore, the chalk, in combining with the acid, is dis- 
solved ; hence, acid-forming colonies are surrounded by a clear zone. 
This clearing of the medium is a valuable aid in recognizing acid- 
forming colonies. 

The medium consists of : 

Gm. or c. c. 

Agar 15 

Liebig's extract 5 

Salt 5 

Peptone 10 

Lactose 20 

Calcium carbonate 4 

Litmus solution 100 

Water 1, 000 

The agar, Liebig's extract, salt, and peptone are dissolved in 1 
liter of water, either in the autoclave or over the free flame. This 
is then cleared with the whites of two eggs and filtered through cot- 
ton. No titration or adjustment of reaction is necessary. The 
medium should then be flasked, 250 c. c. to a flask preferably of 500 
c. c. size. One gm. of powdered calcium carbonate is then added to 
each flask, and the whole sterilized in the autoclave. Finally, to 
each flask is added 25 c. c. of Kahlbaum's aqueous litmus — according 
to Kubel and Thiemann — (or an equal quantity of a solution of 
azolithmine) ; and 5 gm. of chemically pure lactose. Tube by 
pouring direct from flasks to tubes, keeping contents well mixed. 
Sterilize in an Arnold sterilizer for 15 minutes on three consecutive 

In using this medium either surface smears may be made on 
plates or the tubes inoculated and poured. For most uses, the 
poured plates give best results. To obtain a uniform distribution of 
the chalk throughout the medium, the tubes should be rolled rapidly 
to and fro between the palms of one's hands, and then by alternately 
depressing and raising the plugged end of the tube, combining this 
with a rotary motion. This mixing should be done as soon as tubes 


are melted and while still hot. They are then cooled to 42° C. They 
may then be inoculated and poured. 

Inoculated plates may be incubated 14 to 48 hours at 37° C, or 
from 2 to 5 days at room temperature. Usually 18 to 24 hours at 
37° C. gives best results. 

Acid production in this medium is shown by : 

1. Dissolving of the chalk about the colony due to its combination 
with the organic salts. 

2. Keddening of the colony due to the litmus. 

3. Microscopically, by the deposition of crystals of the calcium 
salts of the organic acids. 

Differentiation between colon and typhoid colonies on this medium 
is readily made. 


1. Surface. — These are large disk-shaped colonies, slightly de- 
pressed in the media. There is a variable amount of clearing about 
them, due to the solution of the chalk. The extent of clearing de- 
pends on the length of time the plates are incubated. Microscopi- 
cally, on focusing up and down, the chalk is seen to be dissolved just 
below the colony and about its periphery. Crystals of the calcium 
organic acid salts are usually seen. 

2. Deep. — These are rounded or spindle-shaped, showing a very 
distinct clearing of the chalk for a considerable area about the 


1. Surface. — These are large white or bluish- tinged colonies show- 
ing no clearing of the chalk. Microscopically, the amorphous gran- 
ules of the chalk are seen to be both within and about the colony. 
No crystals of the organic salts are present. 

2. Deep. — These are distinct colonies lying embedded in the chalk, 
without solution of the chalk occurring. 

For isolating the typhoid bacillus from feces, sewage, or contami- 
nated water 1 per cent lactose and 1 per cent saccharose may with 
advantage be substituted for the 2 per cent lactose. Plates should 
be incubated 14 to 20 hours at 37° C. Suspected typhoid colonies 
should be fished and inoculated into Hiss tube media or other 
suitable media for identification. I have on several tests isolated 
typhoid bacilli direct from the feces without enrichment. 

The advantages of this medium are : 

1. Neutralization of the acid as it is produced. 

(A) Crowded or well-diluted plates may be used with equal ad- 

(B) The period of incubation is not limited. 


(C) Acid formation is more clearly shown and its extent may be 

2. Simplicity of the medium : 

(A) Stock meat extract may be used by simply adding chalk, lac- 
tose, and litmus. 

(B) The medium is neutral in reaction to litmus without titra- 
tion or adjustment, The acidity of meat extract is neutralized by 
the chalk, giving a neutral agar on which slight alkalinity or acidity 
is readily shown. 

This type of medium may be used in growing and identifying any 
organism in which the fermentation of any sugar is the base of its 
differentiation. For some organisms, such as the pneumococcus and 
streptococcus, meat infusion agar may be substituted for the meat 
extract agar. Any of the sugars may be used instead of the lactose. 
The percentage of sugar may be varied from 1 to 5 per cent. 


Anna W. WiIliams, from the Division of Laboratories (director, Wm, H. 
Park), Department of Health, New York City. 

In February, and again in December, 1911, the writer published 
reports of growing amoebae isolated from the intestines of mammals 
on tissue culture media without the presence of other microorganisms. 
So far as the author knows, these are the only reports of growing, 
successively, strictly pure cultures of amoebae. These pure cultures 
are comparatively easily obtained. The conditions are, simply, strict 
asepsis in removing the tissues and sufficient controls in transplant- 
ing the cultures to be sure of being rid of the ubiquitous air germs, 
of those growing originally with the amoebae, and, lastly, of those 
sometimes circulating in the blood of the animals chosen for the tissue 

In carrying on the work further, some interesting points have come 
to light in regard to the life history of these organisms which may be 
mentioned now, though the study is incomplete. Only one of the 
strains of amoebae originally used has been chosen, and its life cycle 
has been studied in these pure cultures under varying conditions 
(amoeba 11524 from Manila). This culture is now in its seventieth 
culture generation on brain media. 

The brain medium among the three tissue media found suitable — 
i. e., brain, liver, and kidney — seems to be the best for abundant and 
continuous growth; therefore, this has been used exclusively in the 
further studies. 


A most important part in regard to these tissue media is that they 
afford a good opportunity of studying amoebae in cultures under 
conditions at least approaching some of the more important ones 
found in the intestines, such as continued high temperature combined 
with much moisture, some lack of oxygen, and the presence of cell- 
division excitants. These conditions have apparently been little con- 
sidered by previous investigators, and not at all by some of the more 
recent ones, in their culture studies, though such conditions must 
obviously be of marked influence in the life history of any protozoan ; 
and, if so, it seems to the author that to compare so-called strict para- 
sitic forms, seen in preparation directly from the intestines or tissues 
of mammal hosts, with culture forms grown under conditions, far 
removed from those obtaining in these mammals, is, to say the least, 

Until such comparative studies are made the question of the rela- 
tionship between the so-called strictly parasitic and pathogenic 
amoebae and the so-called free-living forms, among which have been 
included by all of the most recent writers the culture amoeba, must 
remain an open one. 

It is not surprising that these writers have obtained only the 
results with their cultures that they have reported, for they have 
grown their amoebae on the surface of more or less rapidly drying 
agar, with one or two varieties of bacteria, at a temperature much 
below that of the body. Under these conditions one would expect 
the organisms to pass rather quickly into simple protective cysts con- 
taining one nucleus and showing few other changes. And this, ac- 
cording to nearly all descriptions, is just what they do. 

One investigator, Latham (1911), considered at least some of the 
intestinal conditions and he has reported some suggestive results 
from his culture experiments. Briefly, his work is as follows: He 
worked with two culture strains which came from Manila (numbers 
not designated) and which he called Entamoeba coll. He studied the 
life cycle of these strains with certain auxetics (Ross) or substances 
supposed to be capable of inducing division in living cells. He used 
chiefly tyrosin, leucin, and skatol. He states that on an alkaline agar 
medium containing 0.2 per cent tyrosin a complete life cycle is passed 
through in about three days, as compared with the four-days' cycle on 
Musgrave & Cleggs's medium. In three days all of the amoebae of a 
given generation have encysted. Then a large number of cysts pro- 
duce eight daughter forms inside of them, and the amoebulae come 
out of their cysts and start a new generation on the same medium. 
This has been seen through five generations. This important com- 
munication, unfortunately, does not go into details, but, until such a 
time as it may be disproved, it must be regarded as evidence that 


amoebae in cultures may show schizogony similar to that described 
for Entamoeba coli in intestinal contents. 

Now, as to the original work. In the first place, the fact must be 
emphasized that the strain of amceba used in these studies, as well as 
many other culture strains, grows readily, abundantly, and continu- 
ously at high temperature (38° C). Whitmore states that he was 
unable to get his culture to grow above 26° C. Most other authors 
simply say they grow their cultures at room temperature, and the 
others do not mention temperature. Growing Amceba 11524, then, 
at continuous high temperature (38° C.), with an adequate supply 
of moisture, and in a mass of brain tissue which supplies sufficient 
food and partial anaerobiosis, the following results are obtained : In 
the first 48 hours the amoeba? (planted from a number of trophozo- 
ites) grow and divide rapidly. They spread over the surface of the 
brain mass and penetrate a certain distance within it. Spreads fixed 
moist in Zenker's fluid, and stained with Delafield's hematoxylin show 
trophozoites somewhat similar to those described for culture forms 
by other authors, except many more mitotic figures are seen if the 
amoebae happen to be well fixed and stained. In three days there 
are a number of forms showing two fully developed nuclei and occa- 
sionally one showing three; the organisms are larger and may be 
somewhat vacuolated, and the chromatin about the periphery of the 
nucleus is much larger in amount. In four days there are many very 
large forms which show two nuclei, and some three and four. The 
peripheral nuclear chromatin in some has markedly increased. 
These forms are apparently in good physical condition, as on sub- 
culture they seem to be normally motile, and they divide in a short 
time into daughter amoebae. A number of forms have encysted, and 
among these a goodly number show two nuclei. Even so far we 
find that the results are quite different from those reported by Whit- 
more, Walker, Craig, and others for their culture forms. They all 
state that the cysts in their cultures contain only one nucleus. In 
five days, unless some substance is added to excite the amoebae to 
renewed growth, there are more encysted forms on the surface of the 
growth, while, a little below the surface of the brain mass, some 
motile forms have begun to show distinct changes in the nucleus and 
cytoplasm — the peripheral chromatin appears to be passing into the 
cytoplasm, and the caryosome is distinctly smaller. The chromatin 
in the cytoplasm appears to be collecting in small masses, some about 
the periphery of the cytoplasm; such forms, as you may see from 
the photograph, present an appearance similar to that described 
from the exogenous sporulation of Entamoeba histolytica. The fate 
of these various forms in pure cultures is" still under observation. 


Now, if to a three-day pure brain tissue culture some bacterium 
suitable for food for the amoebae be added in small enough amounts 
to prevent an immediate overgrowth of the bacterium at the high 
temperature used, the amoebae grow and divide with marvelous 
rapidity, and in such cultures we find, in the next two or three days, 
the majority of the amoebae containing two, three, and four nuclei, 
some containing five, and a few containing six nuclei. Unfortunately 
I have not yet been able to get good photographs of these, partly 
because these forms take up the stain so readily and partly because 
the nuclei are often not in the same plane. In these cultures many 
forms have large vacuoles, and a series of forms has been observed 
corresponding to that described by Schaudinn and others as autog- 
enous conjugation in Entamcvha coll. In these cultures, also, definite 
cysts containing four and five nuclei have been found. 

These observations are being continued. I wish only to state at 
present that, so far, these studies starting with pure cultures of an 
ameba obtained from intestines of man have lead us to the following 
conclusions : 

1. That when conditions of temperature, anaerobiosis, moisture, 
and food supply in certain culture amoebae are varied, so as to be 
more in accord with conditions found in the intestines and tissues of 
amceba hosts, appearances may be produced which seem to be similar 
to many of those described as important in the entamoeba group. 

2. That this fact opens up anew the question of the relationship 
between the "parasitic forms" (Entamoeba) and the "free-living 
forms" (Amoeba). 


Capt. Charles F. Craig, Medical Corps, United States Army: 
These observations of Dr. Williams are suggestive and important 
as showing the effects of environment upon cultural amoebae. How- 
ever, I do not believe that they prove that cultural amoebae are enta- 
moebae. or true parasitic amoeba'. According to her description of 
the morphology of this amoebae in the brain media, forms were ob- 
served which resembled slightly all three entamoebae of man — coli, 
histolytica, and tetragena. Of course, such an observation as this 
is most confusing and, I believe, indicates that the developmental 
forms showing such appearances are abnormal and have no relation 
whatever to true parasitic amoebae. Practically all protozooloists who 
have studied sufficient material agree in considering the cultural and 
parasitic amboebae as entirely different, and the modifications in struc- 
ture detailed by Dr. Williams are not sufficient to prove that this 
cultural amoebae has been transformed morphologically into an enta- 
moeba*. The uuclear structure, even in the four-nucleated st;ii2;<\ as 
shown in the photographs, is entirely different from the nuclear 


structure of any of the entamoeba* and still approaches closely the 
typical nuclear structure of the same cultural amoebae when grown on 
Musgrave's medium. 

However, I think that Dr. Williams should be congratulated upon 
having succeeded in obtaining pure cultures of amoeba', certainly a 
great step in advance in the study of this class of organism. 


By Edwin O. Jordan, Professor of Bacteriology, University of Chicago, 

Chicago, 111. 

When the purpose of a bacterial water examination is to determine 
the occurrence, recency, or degree of bacterial contamination of a 
potentially dangerous character, it is generally held that the quanti- 
tative estimation of B. coli furnishes the most satisfactory evidence. 
Konrich, 1 to be sure, in an elaborate critical summary, maintains that 
the coli test is no more than an unnecessary complication of the 
older modes of procedure, but the general experience of water 
analysts with this method, extending in this country over 20 years, 
is strongly in its favor. It is true that the presence of B> coli in 
water is not always due to contamination with material of human 
origin, but many observers have shown that the number of colon 
bacilli in a water does not rise above a certain level — usually fixed 
as about 1 per c. c. — unless exposure to fecal contamination has 
existed. Savage, 2 for instance, was led by his study of a large num- 
ber of water supplies in Wales to conclude that even in surface 
waters exposed to animal contamination from adjacent fields and 
grazing grounds the ratio of B. coli is less than 1 in 2 c. c, unless 
other sources of pollution exist. In the United States the water of the 
Great Lakes is practically free from B. coli, even in 50 and 100 c. c. 
samples, except in the immediate neighborhood of human habitations. 
In the vicinity of large cities, like Chicago and Milwaukee, a zone 
of colon bacilli may extend at least as far as 5 or 6 miles from shore. 
In whatever way the presence and relative abundance of B. coli 
in water may be interpreted there can be no doubt that the absence 
of this organism from quantities as large as 100 c. c. gives more 
direct and convincing evidence of the bacterial harmlessness of the 
water than any other method, chemical or bacteriological. 

For the earliest recognition of the importance of the quantitative 
estimation of B. coli in water, as well as for a practical numerical 
method, we are indebted to Theobald Smith. The fermentation tube 
method devised by him in 1892 is to-day the basis of some of the most 
widely used procedures. 

In the course of some water examinations, I have had occasion to 
make comparative tests of certain of the media in current use or 


recommended for the quantitative estimation of B. coli. One that 
has been widely employed in this country is the lactose 'bile medium. 
An obvious advantage of this method is the inhibition of a number 
of water bacteria thought to be nonsignificant, including gas- 
producing bacteria other than B. coli. This facilitates isolation of 
B. coli and is also asserted to give a higher value to the presumptive 
test. A disadvantage apparently not so generally recognized is the 
inhibiting effect of the bile upon genuine colon bacilli. It is ad- 
mitted that the bile exerts some restraining effect upon the " weaker " 
cells of this species. The last report of the committee of the Ameri- 
can Public Health Association on "Standard methods of water 
analysis" (1912, p. 88), states that "it has been found that the 
lactose bile medium is slightly inhibitive to B. coli, especially in 
attenuated form." In point of fact, inhibition also of freshly 
isolated strains of B. coli occurs to a noteworthy degree. This sup- 
pression of freshly isolated fecal strains in pure culture on bile agar 
has amounted, in my observations, to from 30 to 65 per cent. A 
series of tests made with lactose bile fermentation tubes on fresh 
sewage in 1 : 100,000 dilutions has given positive results in only about 
45 per cent of the samples in which B. coli was present, using lactose 
broth enrichment tubes, plating, and complete identification as a 
standard. In a word, the use of the bile medium may lead to the 
suppression of at least half of the viable cells of B. coli present in 
freshly isolated fecal cultures and in fresh sewage. 

It may be noted here that an increased percentage of positive 
results will be obtained from lactose broth, used as an enrichment 
medium for B. coli, if a number of colonies are fished after plating, 
and especially if the contents of the fermentation tube are replated 
after an initial negative result. In one series of observations, made 
on Lake Michigan water, B. coli was not infrequently isolated on 
replating from lactose fermentation tubes which, in the first trial, 
had given negative results. Approximately one-fourth of the tubes 
examined in this way finally yielded typical B. coli. It is well 
known also that B. coli does not always produce typical colonies on 
litmus lactose agar, and that further identification kests are neces- 

I have also used Endo medium for comparison with lactose broth, 
plating two samples, of 5 c. c. each, direct in this medium, and com- 
paring with ten 1 c. c. samples in lactose broth fermentation tubes. 
Ninety cubic centimeters of Lake Michigan water, examined in this 
way, have yielded, by the lactose broth enrichment method (plating 
in litmus lactose agar and subsequent identification), 34 cultures of 
B. coli while the parallel samples on Endo medium have given 36 
identified cultures. Not all the colonies on Endo medium resem- 
bling typical B. roll prove to be B. coli on further examination. Of 


102 colonies fished and examined, 72 proved to be B. coli. Twenty- 
nine picked as negative were all negative. On the other hand, 12 
out of 61 colonies picked as doubtfully resembling B. coli turned 
out to be characteristic B. coli. As a presumptive test, therefore, 
simple enumeration of the colonlike colonies on Endo plates is no 
more reliable than the lactose bile or lactose broth methods. In this 
respect my experience agrees with that of Frost 3 rather than that of 
Schiirer. 4 

In general, it would seem that a plating method would be prefer- 
able to a dilution method. The Endo medium is much more valu- 
able for direct plating than litmus lactose agar, since overgrowth 
occurs but seldom, and the colony differentiation is sharper. In an 
attempt to combine these advantages with rapid identification, I 
have obtained excellent results by picking colilike colonies from 
the Endo medium, and transferring to Russell's medium and gelatin. 
Nearly all colonies giving a positive reaction in Russell's medium are 
typical for B. coli in gelatin, but a few of uncertain systematic posi- 
tion (8 in 116) liquefy gelatin. As already stated, some of the 
colonies on Endo medium, that are unlike B. coli, or that doubtfully 
resemble the latter, yield positive reactions when transferred, but 
further investigations should permit a pretty accurate estimation 
of the proportion of such forms. 

To summarize briefly : Bile media are not properly selective, since 
a considerable and varying proportion of the cells of B. coli do not 
develop in them. This is true not only of media, to which natural 
bile is added, but also, although to a lesser degree, of media such as 
MacConkey's, which contain the purified bile salts. Simple lactose 
broth in fermentation tubes, although not open to objection on this 
score, permits the development of so many gas-producing bacteria 
of uncertain sanitary significance that plating out and identifica- 
tion will generally be considerd necessary. Direct plating on Endo 
medium allows the use of #f airly large amounts of water, does not 
inhibit any viable cells (so far as comparison with ordinary nutrient 
agar indicates), and leads to characteristic colony formation in the 
great majority of cases. Transfer of selected colonies to Russell's 
medium and gelatin permits a fairly rapid and complete identifica- 
tion. Compared with the more roundabout and time-consuming 
method of enrichment in lactose broth and subsequent plating, the 
procedure here outlined gives almost exactly the same proportion 
of positive results, and is simpler and quicker. 

'Klin. Jahrb., 1910, 23, p. 1. 
2 Jour, of Hyg., 1902, 2, p. 320. 

8 Bull. No. 78, Hyg. Lab., U. S. Pub. Health and Mar. Hosp. Service, pp. 
4 Ueber den Nachweis des B. coli iin Flusswasser, Inaug. Diss., Gottingen, 1910. 
66692— vol 2, pt 1—13 i 



Prof. Dr. Gartner (Jena) sagt, dass in Deutschland noch immer 
die Untersuchung der Lokalitat an erster Stelle stehe. Die Abwesen- 
heit von Colibacillis gibt nur an, dass zu Zeit keine Infections- 
gefahr vorliegt, aber sie sagt nichts ftir die Zukunft. Ausserdem ist 
das atypische Coli ebenso haufig im Darm von Menschen und Tieren 
vorhanden als das typische. Das Bact. coli hat in manchen Fallen 
eine grosse Bedeutung, in anderen nicht. 

Dr. F. L. Rector (Brooklyn, N. Y.). During the past year some 
work has been done in my laboratory, using a medium of dried ox- 
bile peptone, lactose agar, and neutral red. This is used in direct 
planting work, and on this medium the colon shows as a distinct 
purplish red colony, the color shading off into the denser medium. 
Streptococci may show red, but their colonies are not so large, nor is 
the characteristic color present. In using this medium as a check with 
litmus lactose agar, it was found that 55 or 60 per cent of the colonies 
isolated, not all of which were characteristic, proved to be colon, while 
only 18.5 per cent of those on litmus lactose agar were colon. 

E. O. Jordan. I think there can be no difference of opinion on the 
point raised by Prof. Gartner. In passing judgment on the char- 
acter of a water-supply knowledge of the environmental condition is 
essential. Often examination of the local surroundings gives all the 
information needed. It is not necessary to analyze a river water to 
determine whether it is polluted with sewage if one can see the sew- 
age flowing into it. Under some conditions, however, analytical evi- 
dence is an important aid. It is sometimes uncertain, from simple 
local inspection, whether a water-supply is or is not contaminated; 
the degree of self-purification occurring in a flowing stream can not be 
determined by inspection alone ; in the Great Lakes, mere ocular ex- 
amination can not determine the distance from shore to which danger- 
ous contamination may extend. There are conditions, then, when 
bacterial examination may aid in forming judgment as to the char- 
acter of a water. Such bacterial examinations can not replace the 
environmental inspection; they presuppose it. 

Dr. Wm. H. Park. The practice in America is nearly in accord with 
the opinions of Prof. Gartner. In New York City the description 
of the source of the water supply is always considered together with 
the chemical and bacterial examination. In surface waters a number 
of colon bacilli might not be considered very suspicious, while in 
well or spring water the same number would be very significant. 



Prof. C. C. Bass, Laboratory of Tropical Medicine and Hygiene, Medical Depart** 
ment, Tulane University, New Orleans, La. 

This was a stereopticon demonstration. A paper discussing the 
technique for the cultivation of malarial plasmodia was published by 
Drs. C. C. Bass and Foster M. John's, in the Journal of Experimental 
Medicine, Volume XVI. No. 4, 1912. 


Capt. Chas. F. Craig, Medical Corps, United States Army: 
When I first read of the cultivation of the malarial plasmodia by 
Dr. Bass, I am frank to say that I was very skeptical, but withou£ 
my requesting them, the doctor very kindly sent me a complete set 
of stained preparations containing examples of the complete 
schizogamy of the sestivo-autunmal plasmodinm, and I am prepared 
to state that he has undoubtedly grown them through one generation, 
and in my preparations another generation was apparently beginning. 

I believe that the successful cultivation of the malarial plasmodia 
will greatly aid us in the elucidation of many still unsolved problems 
connected with these parasites. It should be of great value in the 
study of species and perhaps will settle once and for all time the 
question of the occurrence of a quotidian and tertian sestivo-autumnal 
Plasmodium, which is still a matter of controversy among students of 
malarial disease. The early development of the gametes and the 
actual form of the parasites which cause long-term relapses, may 
possibly be studied in these cultures, for it is reasonable to suppose 
that latent or resistant forms would develop even more numerously 
in such cultures than in the patient's blood. In this way we may be 
able to decide whether parthenogenesis, intracorpuscular conjugation, 
or the development of the plasmodiei in small numbers is responsible 
for relapse. The method should be of great value for teaching pur- 
poses, as in this way it will be possible to supply classes with malarial 
preparations, even in regions where the disease does not occur. It is 
needless to say that if these parasites can be cultivated through many 
generations, great therapeutic results may be obtained by testing the 
effect upon the cultures of various remedial agents, and in this way 
we may be able to discover a specific for malaria more efficient and 
less disagreeable than quinine. 

I was specially impressed with the fact that in the culture the 
polymorphonouclear leucocytes were phagocytic, for in actual mala- 
rial infection it is generally the monouclear leucocytes that are most 



Charles W. Duval, M. D., Tulane University, New Orleans, La. 

(From the laboratories of Pathology and Bacteriology.) 

Since the discovery by Hansen in 1872 of an acid-fast bacillus in 
the leprous lesion to which he ascribed an etiological role, numerous 
investigators have reported success with its artificial cultivation. It 
may be stated, however, that many of the cultures which have been 
isolated and described by various workers so differ in their acid-fast 
property and their morphological features from the Hansen bacillus 
of the tissues that no one of them has been universally accepted as 
the specific organism of leprosy, although many of these cultures are 
said to have induced experimental lesions similar to human leprosy. 

A review of the literature would seem to show that three, and pos- 
sibly four, apparently different germs have been cultivated from the 
leprous lesion and described as the casual agent of the disease, 
namely: (1) A non-acid-fast streptothrix which becomes acid 
fast by passage through the rat (Kedrowski), (2) an acid-fast 
chromogenic bacillus (Clegg), (3) a chromogenic non-acid-fast and 
acid-fast streptothrix (Koss and Williams), and (4) an acid-fast 
nonchromogenic bacillus which grows in vitro only in the presence 
of the amino acids (Duval). 

In the experience of the author two types of acid-fast organisms 
may be cultivated from the leprous lesion which have distinct charac- 
teristics — one, an extremely pleomorphic bacillus, variable in its 
ability to retain the stain after the ordinary methods of decoloriza- 
tion, and multiplies profusely on all media as a moist lemon or 
orange-colored growth; the other, a permanently acid-fast bacillus, 
which grows only upon special foodstuffs and apparently does not 
produce pigment. These two types probably include many of the 
cultures which have been described from time to time as the leprosy 
organism, since the chromogenic variety is often a non-acid-fast 
diphtheroid, streptothrix, etc., depending upon growth conditions. 1 
These tinctorial and morphological variations of the pigment pro- 


ducer might account for the bewildering number of " stages " for 
the Hansen bacillus of some European writers. 

Kedrowski's organism, which he cultivated from the leprous nodule 
and regarded as the specific bacillus of leprosy, he describes as a non- 
acid-fast streptothrix, which becomes permanently acid fast after a 
sojourn for several weeks in the tissues of the rat. He advances the 
theory that the acid-fast rods seen in human leprosy represent but a 
stage in the developmental cycle of a single pleomorphic species. 

More recently Bayon 3 described a non-acid-fast diphtheroid which 
he obtained from a leper that behaved in a manner similar to 
Kedrowski's culture ; i. e., the initial growth from the human tissues 
was non-acid fast until passed through the rat, after which it 
changed into an acid-fast bacillus. He concludes that not only 
is his culture identical with Kedrowski's, but also that it is the 
cause of human leprosy, basing his argument upon specific reac- 
tions obtained with human leper serum and also upon the production 
of lesions in the laboratory animal. It is reasonable to suppose that 
Kedrowski and Bayon were dealing in the beginning with a mixed 
culture which became purified by animal passage, thus accounting 
for the disappearance of the pleomorphic non-acid-fast forms after 
the culture was recovered from the tissue of the experimental animal. 
The non-acid-fast diphtheroid and streptothrical forms, which were 
present in their original cultures from the human tissue, can be 
accounted for in no other way. 

Though I have not compared Kedrowski's acid-fast organism with 
my nonchromogenic strain, it is possible that they are the same, 
since the isolation and cultivation of both were obtained with the 
products of tryptic digestion. Kedrowski used these nutrients, with- 
out apparently knowing it, in the form of placental extract, because 
he does not mention why he used placenta in preference to other 
media, or that it contains the amino acids. Whether Kedrowski's 
organism, since it has become permanently acid fast, is identical with 
my nonchromogenic strain can be determined, of course, by a com- 
parative study of the cultures. 

In regard to the chrome-producing organisms which have been 
isolated from the leprous lesion and thought to be of etiological sig- 
nificance, Clegg's 4 culture is perhaps the most important. He an- 
nounced his success in the cultivation of a chromogenic bacillus which 
he obtained from the specific lesion in a large series of lepers in 
the Philippines. Multiplication in each instance occurred in the 
transferred tissue bits when planted with amoeba? and their symbionts, 
and pure cultures were subsequently secured on the ordinary labora- 
tory media as a moist, profuse, yellow T pigmented growth, by heating 
at 60° C. for 30 minutes to kill out the symbionts. 



Ross and Williams 5 have also reported upon the successful cultiva- 
tion from the leprous nodule of an organism similar to that of Clegg's, 
together with which they found streptothrical forms and acid- 
fast diphtheroids. 

Still other chromogenic cultures similar to Clegg's have been culti- 
vated from the leper by Duval 6 in Louisiana, Brinkerhoff, and 
Currie 7 in Hawaii, Rivas 8 in Philadelphia, Thompson 9 in Australia, 
and Wellman 8 in California. 

I have compared the original chromogenic culture of Clegg with 
those isolated independently by other workers, and have found them 
identical, except the Ross and Williams strain. Careful serological 
tests with immune sera tend to show that they are all closely related. 
Furthermore, the serum tests prove conclusively that these chromo- 
genic cultures are not related to the nonchromogenic strain culti- 
vated from the leprous lesion by me in 1910 ; 10 in other words, they 
are distinct species. 

In a previous paper 1X I regarded the nonchromogenic and chromo- 
genic cultures as one and the same organism; attributing the subse- 
quent alteration in morphology of the culture, its increased rate of 
growth and production of pigment, as within the possibilities of a 
species which had become adapted to an artificial environment. 
The lesions which were induced in the monkey with the chromo- 
genic culture seemed further proof of its specificity, because they 
were indistinguishable from the human lesion. However, I have 
since determined that lesions similar to leprosy can also be induced 
in this animal with many of the well-known saprophytic acid-fast 

That the chromogenic strain exists in the lesion of certain types 
of leprosy, there can be no doubt, even where the overlying skin is 
apparently intact, and also in the internal organs at autopsy. Again, 
the chromogenic species is also the predominating organism in the 
leprous abscess, and undoubtedly accounts for the orange-yellow color 
so characteristic of the pus from this type of lesion. Of course, it is 
well known how ubiquitous are the saprophytic acid-fast species, it 
being possible to isolate them from almost any source. Their occa- 
sional occurrence, therefore, in the open-skin lesion of leprosy is to 
be expected, but to find them so frequently is difficult to understand, 
if we accept that they are in no way concerned in the disease. 

As stated in a former publication, 11 the chromogenic variety has 
been cultivated from 14 out of 29 cases of leprosy in Louisiana; while 
the nonchromogenic strain was recovered from 8 cases. Since it is 
more difficult to cultivate the nonchromogenic species, especially 
where the two exist in the lesion, this probably accounts for the 
larger percentage of case- yielding the chromogenic variety. Further- 


more, the subplants of the chromogen remain for many generations 
within the morphological variations and staining properties of the 
nonchromogenic type, which would not lead one to suspect that he 
was dealing with two distinct species of acid-fasts. 

Prior to 1910, all the attempts to cultivate the Hansen bacillus 
through^ successive generations were carried out upon media contain- 
ing the whole protein. That the initial multiplication of the leprosy 
bacillus in removed tissue bits has been obtained by a number of 
workers there can be no doubt. The failure has been to perpetuate 
the culture through any number of generations. 

The relationship of the leprosy organism to the tissue cells in vivo, 
and its ability to multiply in digested pieces of excised leprous tissue, 
explains, in my opinion, its failure to grow outside of the animal 
body upon a medium which does not contain the products of tryptic 
digestion. It also explains why transplants from a culture which 
contains both the chromogen and nonchromogen to ordinary media 
have resulted ultimately in the growth of the pigment producer ; the 
nonchromogenic type, or true Hansen bacillus, which I believe it is, 
failing to multiply as soon as removed from the amino-acid nutrient. 

Experiments with the amino-acids 10 as a culture medium, and the 
behavior of B. leprae in digested bits of leprous tissue, establishes 
the fact that the organism requires the products of tryptic digestion 
for assimilation, and is unable to attack and break down the whole 
protein. Where multiplication has been noted, the medium un- 
doubtedly contained these important nutrients. Practically in all 
my successful attempts to cultivate the specific organism, the trans- 
ferred pieces of the leprous tissue were responsible for the growth. 
Multiplication occured whenever, for one cause or another, the 
tissue underwent digestion, and, conversely, did not occur if the 
tissue protein remained unaltered short of amino-acid dissociation. 
Usually the digestion was due to the action of some contaminating 
microorganism. I have repeatedly shown this to be the case by pur- 
posely adding to the removed bits of leprous nodle some one of the 
protein-splitting bacteria, and almost without exception the acid- 
fast rods have multiplied as soon as digestion was well advanced. 


The various acid-fast cultures which may be cultivated from the 
human leprous lesion fall into two groups: (*) A nonchromogenic 
bacillus, cultivated with difficulty, and growing in vitro only upon 
special foodstuffs, ( 2 ) a pigment producing pleomorphic organism, 
which is likewise difficult to cultivate through the first generations, 
but subsequently multiplies readily on all merlin. 


Under certain conditions the individual bacilli of the chromogenic 
species are diphtheroid, streptothrical, and nonacid fast, while those 
of the nonchromogenic species are always acid fast and maintain in 
general the morphological variations common for the tubercle family. 

Serological tests differentiate between these two acid-fast types and 
indicate that the slow-growing nonchromogenic variety is the etio- 
logical factor in human leprosy, and that the chromogenic strain 
belongs to the group of saprophytic acid-fast bacteria. 

Since we frequently encounter in the leprous lesion diphtheroidal, 
streptothrical, and other forms of saprophytic species capable of 
changing in vitro under defined conditions, it is easy to explain the 
u stages " described by Kedrowski and also Bayon in the develop- 
mental cycle of the Hansen bacillus. 

I believe that the specific organism of leprosy in culture as well as 
in vivo is nonchromogenic, acid fast, and thus far has been cultivated 
in vitro only upon an amino-acid medium. 

1 Jour. Infec. Diseases, 1912, XI, p. 116. 

2 Ztschr. f. Hyg. u. Infectionskr, 1901, 37, p. 52. 
8 Tr. Soc. Trop. Med. & Hyg. 1912, 5, p. 158. . 

* Philippine Jour. Sc. 1909, 4, p. 403. 

8 Scientific Memoirs of the Government of India, 1911, 42, p. 1. 

8 Jour. Exper. Med. 1912, 15, p. 292. 

7 U. S. Government Reports, 1910. 

8 Personal communication. 
•Australian Med. Gazette, 1912, 31, p. 209. 
10 Jour. Exper. Med., 1910, 12, p. 649. 
u Jour. Exper. Med., 1912. 


Prof. Creighton Wellman, New Orleans : I wish to call attention 
to the success obtained by us in New Orleans using the placental- 
extract-agar devised by myself as a medium for the cultivation of 
strictly parasitic or feebly saprophytic bacteria. When I first de- 
vised this medium, I thought that the idea was a complete novelty. 
I have learned since, however, that Kedrowski suggested in 1902 the 
use of placental juice, although my medium and its method of prepa- 
ration is very different from his original suggestion. In conclusion, 
I wish to say that we in New Orleans at present hold that careful 
consideration is due the nonchromogenic acid-fast leprosy organism, 
discussed in the paper just read. 



Martha;;!.\, m. D., Rockefeller Institute for Medical Research, 

New York City. 

The more general use of lumbar puncture has made it evident that 
influenzal meningitis is a distinct and not infrequent form of sero- 
purulent inflammation of the cerebrospinal meninges. Its clinical 
picture is indistinguishable from the meningococcal and pneumo- 
coccal forms of meningitis, and it is only by cultural demonstration 
of B. influenzae in the fluid obtained by lumbar puncture that the 
diagnosis can be positively made. The mortality rate of influenzal 
meningitis is very high, only 7 patients having recovered from among 
G2 pure cases reported in the literature. 

Influenzal meningitis is more frequent and more fatal among in- 
fants and children than it is among adults. Of the 7 recovered cases, 
only 2 were infants less than 1 year old, though there have been 35 
cases recorded in babies of that age. One of 5 recorded adult cases 
ended in recovery. 

It has been pointed out in a previous paper 1 that the disease some- 
times follows upon undoubted influenzal disease of the respiratory 
tract, and sometimes develops independently of obvious disease of 
that tract. Since the influenza bacillus is often present in the secre- 
tions of the respiratory mucous membrane in children suffering from 
a variety of diseases, during the wide prevalence of influenza, it is 
probable that the infection of the meninges is always secondary to 
respiratory infection and is accomplished chiefly through the blood 
current. Direct infection from the nose can not be excluded and 
should be considered as a possibility. The probability of an ascend- 
ing infection of the meninges from the nasal mucosa is supported by 
the observation that, in monkeys, the influenza bacillus appears in 
the nasal mucus after being injected into the subdural space of the 
spinal canal by lumbar puncture. However, all or nearly all cases 
of spontaneous influenzal meningitis in human beings are examples 
of influenzal bacteremia, since the bacilli have been cultivated in 
large numbers, before and after death, from the heart's blood. The 
same general fact is true of experimental influenzal meningitis in the 
monkey. When the condition is produced by means of a subdural 
injection of a virulent culture, the bacilli can be cultivated during 
life and, at autopsy, from the heart's blood. 


We have succeeded in producing a condition of acute meningitis 
in monkeys that resembles, both clinically and pathologically, the 
spontaneous disease as it occurs in human beings. But only virulent 


strains of B. influenzce can be used to produce such an experimental 
meningitis, the virulence being tested upon white mice, guinea pigs, 
and rabbits. Influenza bacilli isolated from the respiratory organs 
during life or after death are, as a rule, virulent for mice and guinea 
pigs. Of TO strains so tested, only 4 have been found to be devoid of 
all virulence. The case is quite different for the rabbit, since only 
four strains derived from the lungs showed virulence for these animals, 
and in the human patients from whom three of these strains were 
obtained, a blood invasion by the bacilli had taken place. The fourth 
strain was grown in pure culture at autopsy from a lung which 
showed the lesion of influenzal broncho-pneumonia, the blood remain- 
ing sterile. The significance of these facts will be discussed later. 
They are here used to contrast the virulence of the respiratory strains 
with that of the meningeal strains of influenza bacilli, bringing out 
the point that while all the meningeal strains except one (nine in 
number) tested upon young rabbits proved to be virulent, a few 
respiratory strains were found to be just as virulent for these animals. 
Furthermore, so far as our experiments went, it was found, in a 
general way, that bacilli that were virulent for rabbits also proved 
to be virulent for monkeys, and vice versa. 

In the monkeys experimented on the effects of the subdural injec- 
tion of an effective dose of a virulent influenza culture make them- 
selves manifest in about five hours after inoculation. The first 
noticeable effect is a disinclination to move about actively, although 
the monkey may not show severe symptoms for 12 or even 24 hours. 
Death may result as early as 36 hours after the inoculation or it may 
be delayed for three or four days. 


Having produced influenzal meningitis in monkeys, the next step 
was the attempt to treat it. For this purpose an anti-influenzal 
serum from a goat, immunized by means of the injection of virulent 
strains of influenza bacilli during a period of 18 months, was avail- 
able. Injections of this immune serum, made at intervals varying 
from 1 to 24 hours after the introduction of the bacilli into the 
subdural space, cured monkeys after very severe illness. 

The serum is not bacteriolytic in its action, but its opsonic content 
is very high. As a result of the serum injection the influenza bacilli 
in the cerebrospinal fluid are more freely phagocyted, their number 
is reduced, their capacity of growth is diminished, and the eruption 
into the blood is arrested. Along with these effects go cessation of 
the local inflammatory process and progressive improvement in the 
clinical symptoms, usually followed by rapid restoration to health. 




Three human cases of influenzal meningitis have been treated with 
the anti-influenzal serum. 2 The first was an infant 3 months old, a 
patient at the Nursery and Child's Hospital, who developed symp- 
toms of meningitis after an attack of rhinitis, bronchitis, and otitis 
which had persisted for several weeks. On the third day of the 
attack of meningitis 8 cubic centimeters of anti-influenzal serum was 
injected into the spinal canal. In the next 24 hours there was a fall 
in temperature and an improvement in the general condition. The 
following morning 15 cubic centimeters of the serum w T ere injected, 
and within 15 minutes the baby collapsed and died in spite of heroic 
attempts at stimulation. While care had been taken to inject a 
smaller amount of fluid than had been withdrawn, the effect on the 
blood pressure of so young a child was evidently more .serious than 
was indicated by the pulse and respiration. Had Sophian's method 
of watching the blood pressure been employed in this case, the col- 
lapse would probably not have occurred. Pure cultures of B. influ- 
enzae were grown from the cerebrospinal fluid and from the pus of 
the middle ear, while the bacilli were also present in the nose and 

The second case came under the observation of Dr. C. H. Dunn, of 
Boston. A girl of 4 years had had symptoms of irritability and 
headache for two weeks before convulsive twitchings began. Two 
days later, the diagnosis having been established bacteriologically, 
anti-influenzal serum was injected, and the dose of 30 cubic centimeters 
was repeated three times. At first an improvement in the pulse and 
temperature was noted, but death occurred on the seventh day. 
While the cerebrospinal fluid had become more cloudy as the disease 
progressed, phagocytosis became marked after administration of the 
serum. B. influenza' was grown in pure culture from the cerebro- 
spinal fluid before death and from the meningeal exudate and heart's 
blood at autopsy. 

The third case was that of a boy 13 months old, admitted to the 
Babies' Hospital on the third day of his meningitis, which followed 
an attack of pneumonia. After two injections of the anti-influenzal 
serum the temperature, pulse, and general condition were greatly 
improved, and the serum was omitted for a day. Then a rise of 
temperature occurred, convulsions became severe, and death ensued 
on the sixth day. At the autopsy an extensive lepto-meningitis and 
purulent ependymitis were found. B. influenzae was cultivated from 
the cerebrospinal fluid during life and from the meninges, heart's 
blood, and lung after death. 

These results are not entirely discouraging. In all three patients 
decided improvement followed the administration of the first dose of 


the anti-influenzal serum, which, we believe, was not strong enough 
for use in the small doses which must of necessity be given to young 
children if untoward effects are to be avoided (as in case 1). A horse 
has now been immunized for about a year and its serum gives a 
higher opsonic index than was ever obtained with the serum of the 
goat. We are encouraged to hope that the anti-influenzal horse serum 
will yet prove effective in curing human cases of influenzal 



It is necessary to say a word as to the relation of the bacillus 
isolated from our cases of influenzal meningitis with the so-called 
Bacille meningite cerebro-spinale septicemique of Cohen. 3 

Cohen insists that the two bacilli are not identical and that the 
disease is not influenzal meningitis, but cerebrospinal septicemic 
meningitis. He admits the morphological and cultural identity of 
the two organisms, but finds differences in their agglutinative, con- 
glutinative, and protective powers and, above all, in their pathogenic 
effect upon laboratory animals. In my hands, serum reactions with 
B. inftuenzce have been unsatisfactory as a means of differentiation 
of strains. That is, agglutination tests, opsonic tests, and protection 
tests with immune goat serum have given identical results, whether 
made with virulent meningitis strains or with a perfectly innocuous 
strain cultivated from the throat of a child with mild influenzal 

As to the virulence of influenza bacilli, strains of B. influenzce 
freshly isolated from the throat, nose, or bronchial secretion of 
patients suffering from influenza, with or without pneumonia were, 
with few exceptions (4 of 70), virulent for mice and guinea pigs, 
but not for rabbits. On the other hand, all but on strain isolated 
by us from the cerebrospinal fluid in cases of meningitis were viru- 
lent for rabbits, and Batten 4 reports a recovered case of influenzal 
meningitis in a child 14 months old, from whose cerebrospinal fluid 
he isolated a strain of B. influenzce which proved to be entirely with- 
out virulence for mice, guinea pigs, and rabbits. No blood cultures 
are mentioned. In all our cases of influenzal meningitis the virulent 
bacilli were found in the heart's blood before or after death, or both. 
It is a well-known fact that it is rare to find B. influenzce in the 
heart's blood in routine autopsy cultures, Wohlwill 5 having failed to 
find it among several hundred autopsies at the Eppendorfer Kranken- 
haus. At the Babies' Hospital during a period of four years, among 
753 autopsies, it was encountered only eight times, five times in 
influenza] meningitis and three times in cases of influenzal pneu- 


monia with normal cerebrospinal membranes. It is an interesting 
fact that these three respiratory strains were as virulent as any one 
of the meningeal strains and that they entered the general circulation, 
both in the human cases from which they were cultivated and in the 
animals inoculated in the laboratory. That the children did not live 
long enough to develop meningitis is possible. Had they done so the 
bacilli would be classified as Bacilli meningite septicemique, while at 
present we must regard them as virulent strains of B. influenzae. 
That the influenza bacillus does invade the blood stream was ad- 
mitted by Pfeiffer when he so identified the bacillus Slawyk 6 had 
isolated from the cerebrospinal fluid, blood and joint pus from a 
case of influenzal meningitis in 1899. A most interesting case in this 
connection was one of broncho-pneumonia, seen at the Babies' Hos- 
pital, in which the influenza bacillus was isolated in pure culture 
from the lung at autopsy while the heart's blood remained sterile. 
This strain of B. influenzal was virulent for rabbits and guinea pigs, 
and proves that virulence may be an attribute of influenza bacilli 
found in the respiratory tract, whether or not such bacilli enter the 
general circulation. That such bacilli do enter the blood without 
causing seropurulent meningitis is shown by the other three cases 
cited, as well as by the following one: A boy 9 months old was ad- 
mitted for lobar pneumonia, and a blood culture made with blood 
obtained from the external jugular vein on the fourth day of the 
disease proved to be negative, but on the ninth day both pneumococci 
and influenza bacilli were found in the child's blood. On the twelfth 
day the culture was again negative and the child made a perfect re- 
covery without any symptoms of meningitis. The influenza bacillus 
isolated from his blood proved to be virulent for rabbits. 

It should not be forgotten that tests for virulence, to be of value, 
must be made with the earliest generations of B. influenzal immedi- 
ately after isolation from a human lesion. Like other bacteria, this 
bacillus loses its virulence on artificial cultivation outside the body. 

Instead of making a distinct separation of the bacillus of sep- 
ticemic meningitis from the influenza bacillus, it would seem to be 
simpler, and in keeping with all the facts, to say that while the 
majority of influenzal infections of the respiratory tract are due to 
nonvirulent bacilli, such infections are occasionally due to virulent 
strains, and that a virulent respiratory infection may become a 
general one, with or without inflammation of the cerebrospinal 
meninges. Moreover, nonvirulent influenza bacilli have been culti- 
vated from cases of cerebrospinal lepto-meningitis. The virulence 
referred to here is the power to kill young rabbits of about 1,000 
grams weight within 24 hours after an intravenous inoculation of one 
blood agar slant culture of 24 hours' growth, suspended in 1 cubic 


centimeter of salt solution, the influenza bacillus being recovered in 
pure culture from the heart's blood and organs of the animal. 


Influenzal meningitis can be produced in monkeys by means of sub- 
dural injection of virulent influenza bacilli. 

The experimental disease can be cured by means of subdural injec- 
tions of anti-influenzal immune serum. 

Three human cases treated with the serum showed temporary 
improvement, but none recovered. 

From the fact that virulent influenza bacilli are sometimes found 
in lesions of the respiratory tract, whence they may enter the blood 
without causing meningitis, while virulent influenza bacilli are 
sometimes found in the cerebrospinal fluid in cases of meningitis, it 
would seem that a separation of B. influenzas from Baeille meningite 
cerebro -spindle septicemique (Cohen), on the ground of virulence, is 
not possible. 

1 Wollstein, Journal of Exp. Med., 1911, xiv, 73. 

2 1 am indebted to the house staff of the Nursery and Child's Hospital and of 
the Babies' Hospital and to Dr. C. H. Dunn, of Boston, for the history of these 

3 Cohen, Annales de l'lnst. Pasteur, 1909, xxiii, 273. 

4 Batten, F. G. The Lancet, 1910, I, 1677. 
5 Wohlwill, Munch, med. Wochens., 1908, LV, 328. 
6 Slawyk, Zeits. f. Hyg., 1899, XXXII, 443. 



Philip Hanson Hiss. Jr., M. D., Professor of Bacteriology, College of 
Physicians and Surgeons, Columbia University, New York. 

In the past most workers have, in their study of infection and 
their search for biological therapeutic agents, directed their energies 
to the production of specific antisera and have, with few exceptions, 
neglected to approach the question of the treatment of infections from 
the side of the intracellular resisting agents of the system. In many 
infection-, however, the ultimate weapons of defense of the system 
are the leucocytes, either in their normal state, acting as phagocytes, 
or possibly when breaking down in the circulation or in exudates. 


It seemed to me therefore probable that we have certain diseases, 
not especially amenable to serum treatment, in which the ultimate 
immunity or defense is largely cellular, not only in the sense of 
phagocytosis and digestion, but in the neutralization or destruction 
of poisons which are formed by the bacteria or arise from the disin- 
tegration of the bacteria and their products — a mechanism in which 
the protecting cells or their products after their disintegration must 
intervene and, largely unaided by antitoxic bodies in the plasma, 
neutralize the poisonous products of the invading microorganisms. 

It was this thought that suggested to me the idea of treating dis- 
ease by aiding the leucocytes by furnishing them as directly as possi- 
ble with the weapons which were being taken away from them in 
their fight with invading microorganisms, and to protect them thus 
from destruction and give them an opportunity to recuperate and 
carry on successfully their struggle against the invading germs. These 
weapons, whatever might be their nature, I assumed might possibly 
be furnished by an extract of the active substances of the leucocytes 
themselves — substances not ordinarily given up to the plasma or 
serum — and I also assumed that extracts would be more efficacious 
than living leucocytes themselves, introduced into the infected ani- 
mal, since, if diffusible, they would be distributed impartially to all 
parts of the body by the circulatory mechanism and, as quickly as 
absorption would permit, relieve the fatigued leucocytes and pro- 
tect, b}^ any toxin-neutralizing or other power they might possess, 
the cells of highly specialized functions. 

This idea of immunity differs from one that simply assumes the 
cells as the source of all immune bodies, in that it takes into consider- 
ation the presence and production in the leucocytes of agents which 
are not normally given up to the plasma, but which are able to 
reproduce themselves and carry on the functions of coagulation, of 
digestion, or of neutralization simply for the benefit and protection 
of the individual cell, while not being secreted or excreted by the 
cells for the more general benefit of the cell community at large. 

It seemed to me that when these sources of protection are over- 
taxed or fail to act efficiently, the most reasonable course is, if possi- 
ble, to support the system by introducing into the infected animal 
or man the substances composing the chief cells or all the cells of an 
exudate from normal or immunized animals in the most available 
and diffusible form, as little changed by manipulation as possible. 3 

Most other workers on this subject have been chiefly interested, 
apparently, in elucidating the direct germicidal action of certain 
leucocyte extracts on bacteria, and in bringing out differences between 
the serum bactericidal bodies and the bactericidal bodies of the 
leucocytes — in other words, with the mechanism of the bactericidal 
activities of leucocytes as shown in vtiro and in the peritoneal cavity. 


Attempts to influence infection by the use of organ extracts have 
also been made, apparently with little success. The thought, how- 
ever, underlying most of this work differs from my own, as these 
experimenters have adopted such a course, arguing that certain or- 
gans may be. the source of true antitoxins, or of the so-called immune 
bodies — amboceptors — and simply contain them in greater quantity 
than does the serum. 

My work, on the other hand, as I have endeavored to make clear, 
has been based on another conception, and has had, as its immediate 
object, the practical determination of the curative effects of such 
extracts. These experiments and their practical applications have 
now extended over five and a half years. 


Passing now from these questions of theory, I will outline briefly the 
result of the treatment of infections in animals with leucocyte ex- 
tracts. These infections or poisonings have usually been brought 
about by intravenous inoculations and, as a rule, the treatments with 
extract have been given subcutaneously, although at times intraperi- 

The infections to which I wish to call attention chiefly in the 
experiments on animals are staphylococcus, streptococcus, pneu- 
mococcus, typhoid, dysentery, meningococcus, and cholera. 

Staphylococcus infections in animals. 2 — If we analyze our series of 
staphylococcus infections, we find that animals receiving subcutane- 
ous injections of rapidly fatal doses of Staphylococcus pyogenes 
aureus can generally be saved by treatment with the extract of nor- 
mal leucocytes of rabbits, even in small doses, especially when these 
are given intraperitoneally. When intravenous injections of staphy- 
lococcus are practiced, the results are different, but treated animals 
usually survive the controls many days, and present modified histo- 
logic pictures. 

Streptococcus infections in animals. — In experiments with strepto- 
coccus infections I have worked only with those brought about by 
intravenous injections. In these experiments we find a marked 
lengthening of life and even a survival of the treated animals, and 
better results in the animals treated early than in those treated late. 
All of the animals which lived long enough developed articular or 
periarticular lesions, which tend to distinguish these infections from 
pneumococcus infections, which, as we shall see, seldom or never give 
rise in rabbits to such localizations. 

Pneumococcus infections in animals. — If, in my series of experi- 
ments on pneumococcus infections, we consider the animals treated 
with the extract of leucocytes of normal rabbits, we find that in such 


animals an infection, surely fatal in untreated rabbits, becomes sig- 
nificantly modified in treated animals, even if this treatment be 
delayed many hours. Thus, out of 8 control animals used in four 
experiments in which the intravenous infecting dose was the same, 
all died, averaging only 45 hours of life after being infected. Of 
the animals treated — some as late as 24 hours after infection — 9 out 
of 12, or 75 per cent, survived the infection, three died with an 
average life of 60 hours after infection, two of them not having 
received treatment until the expiration of 24 hours. 

These are not selected examples, but are records of events as they 
developed in our regular research tests, and have been fully confirmed 
by experiments undertaken in elucidation of other points, and are 
unmistakably indicative of the powerful beneficent action of such 
extracts on pneumococcus septicemia in rabbits. 

On the other hand, living leucocytes, introduced subcutaneously. 
or even peritoneally, have little or no effect on systemic infections. 

Typhoid infections in animals. — We find that typhoid infections, if 
indeed we may really call them such, in rabbits are essentially differ- 
ent from those caused by such organisms as staphylococci, strepto- 
cocci, and pneumococci. The animals seem rather to suffer an acute 
intoxication, from which they either die within a very limited time, 
when organisms may be recovered from them, or recover completely, 
or go into a state of cachexia, but without organisms in the blood or 
organs. In my experiments the animals, as is usual after toxic doses 
of typhoid bacilli, showed signs of poisoning, remaining quiet and 
refusing all food for some hours. The animals receiving protection 
with leucocyte extract, shortly after this treatment, usually seemed 
worse than the control, and to the inexperienced would appear the 
most likely to die. This might possibly be due to a more rapid 
liberation of toxic substances by enhanced bacteriolytic processes, 
either brought about by a fuller complementing of immune bodies 
by the extract, or by special digestive bodies of the leucocytic ex- 
tract, or it might be due to a somnolent state following a relief from 
active poisoning. That the poisoning in reality was fundamentally 
less severe than in the more normal-appearing control is, however, 
shown by the return of the treated animals to normal condition and 
weight, the weights following a perfectly logical order — untreated 
animal, animal treated late, animal treated early, as is illustrated 
by the following examples: A rabbit of 1,125 grams weight received 
a large but not immediately fatal dose of typhoid bacilli intra- 
venously on April 8, which dose was repeated on April 15 and 22, the 
animal dying on April 29, weighing 895 grams; while another rabbit, 
weighing 1,108 grams, received the same amount of typhoid bacilli, 
but treated with leucocyte extract within five hours after the infect- 
6G()92— vol 2. ft 1—13 5 


ing dose, lost no weight and recovered; and a 1,104-gram rabbit, 
treated each time within one hour, actually gained 200 grams. 

In this experiment no organisms were alive in the control, so that 
the animal died from poisoning and interference probably with 
metabolism and excretion due to cellular changes. 

In another experiment the dose of typhoid bacilli was so toxic 
that the temperature fell immediately instead of rising. The effect 
of the extract in the early-treated animal was not a further lowering 
of the temperature, but an arrest and more abrupt rise than in the 
control and the animal treated after five hours. Furthermore both 
the control and the later treated animal had bad diarrhea within two 
hours, but the animal treated in one hour did not have diarrhea. 

Such experiments with leucocyte extracts on typhoid infections in 
rabbits are sufficient for illustration, and the conclusion from them 
seems unavoidable that leucocyte extracts have a remarkably bene- 
ficial modifying action on the course of typhoid infections or poison- 
ings in rabbits. 

The same holds true in infections in guinea pigs treated with rabbit 
leucocyte extracts, but, apart from noting the fact here that subcu- 
taneous injections, used curatively, are active in guinea pigs, it does 
not seem of import to detail such experiments at this time. 

Meningococcus infection in animals. — In meningococcus experi- 
ments rabbits suffer marked intoxication, if not, indeed, in some in- 
stances a true infection, when given sufficient quantities of almost 
any race of meningococcus intravenously. During the epidemic of 
cerebrospinal meningitis occurring in New York several years ago 
I proved this to my satisfaction many times, so that for the pur- 
pose of the following experiments I had no hesitation in selecting 
rabbits as the test animal. 

If we analyze briefly the results of our experiments on rabbits 
infected with meningococcus, we find the following : In every experi- 
ment the controls died. 

The total number of control animals used in the experiments, in 
which the treated animals received normal leucocyte or immune 
leucocyte extract, was eight. These eight controls, averaging 1,254 
grams, died with an average life of 20 hours after infection. 

Of the treated animals there were 13; 9 of these- recovered, and 4 
died, over 70 per cent of recoveries. 

The average weight of the 9 animals which recovered was 1,200 
grams, and of the 4 which died 1,062 grams, 200 grams lighter than 
the controls, with an average life after the infection of 5.7 days. 

The majority of the animals did not receive treatment until the 
expiration of 5 hours after inoculation, and a number of them not 
until 21 to 24 hours, some of the controls having at times died before 


these animals were treated with leucocyte extract. Severer tests 
could hardly be devised, and when the results of such tests are com- 
pared with those attained with the use of serum they point strongly 
to the value of leucocyte extract in the treatment of this infection. 
Cholera and dysentery infections in animals. — Experiments with 
cholera infection of guinea pigs and rabbits, and with infections due 
to either type of the dysentery bacilli in rabbits, which always proved 
fatal in the control animals, have shown that these infections yield to 
treatment with leucocyte extract in much the same manner as do the 
infections to which I have already called attention. 


The character of the exact action of the extracted substance in 
these various infections is, of course, at present largely a matter of 

The fact that treated animals, in some instances, appear more in- 
toxicated than the untreated may indicate an enhanced lytic action and 
liberation of toxic substances from the bacteria, thus suggesting the 
presence in the extract of complementing bodies, or of digestive bodies 
peculiar to the leucocytes. Such bodies are, of course, known to be 
present and may play an active part, but the strongest impression 
given to one carefully following the experiments and noting the im- 
mediate effect on temperature and the conservation and quick return 
to normal weight of the treated animals is that the principal sub- 
stance at work is one active in neutralizing poisons or preventing 
their formation, and thus able to relieve the animal economy and give 
the phagocytes an opportunity to carry on their work of ingesting 
the microorganisms and their nonsoluble products, thus perma- 
nently rendering them harmless. 

The points which to my mind at present speak most strongly for 
the explanation of the beneficial action of leucocyte extracts, as 
either poison neutralizing or poison prohibiting, rather than pri- 
marily bactericidal or bacteriolytic, or even one of immediate 
phagocytosis, are, first, the effect on temperature; for, when the tem- 
perature is high, it tends to be lowered, and, when it is falling below 
normal from the intensity of the poisoning, it tends to rise on treat- 
ment, which is a sign, of course, under this condition, of returning 
strength on the part of an animal; and, secondly, the effect in pre- 
venting diarrhea, which is a sympton of poisoning in such intoxica- 
tions. Animals treated in time rarely show diarrheal symptoms. 
Mow, if the action of the extract were a poison-liberating one, we 
might possibly have a falling temperature when it is high, following 
the introduction of extract, caused by a further poisoning, but we 
should not have a rise in temperature in an already fatally intoxi- 


cated animal; in the same way, if poison were liberated, animals 
receiving treatment should evince symptoms of diarrhea before the 
untreated ones. And, further, the experiments performed by Zinsser 
and myself in vitro, and in the peritoneal cavities of guinea pigs, 
strongly favor a toxin-neutralizing or coagulating action; for we 
were able to show, in a fairly satisfactory manner, that bacterial 
extracts were precipitated by leucocyte extracts, and we were unable 
to determine any marked extracellular intraperitoneal destruction 
even of such sensitive organisms as cholera vibrios, or, in fact, any 
immediate increase in phagocytosis; and yet the animals were better 
off than the controls. That the action is one affecting the poisons 
immediately, no matter what the effect on the bacterial cells may be, 
seems an unavoidable conclusion, since falls of temperature of several 
degrees may occur within a half hour to an hour after subcutaneous 
adminstration of leucocyte extract. This fact also practically rules 
out an explanation of the extract as being simply a stimulator of 
general leucocytosis from the leucocyte- forming bases of the animal; 
for, even if such a leucocytosis could occur in so short a time, we know 
from experiment that freshly obtained living leucocytes, when in- 
troduced into an infected animal, even intraperitoneally, are prac- 
tically without effect on systemic infections. The lives of the animals 
are not lengthened and these intact leucocytes seem to have no in- 
fluence on the temperature. 

Intravenous injections of living leucocytes have not been tried, 
since the results of such a procedure are of purely academic interest, 
being entirely outside the realm of possibility in the treatment of 
human infections. The use of living leucocytes in the treatment of 
local infections is, of course, possible, but of limited application, 
both theoretically and practically, and their beneficial action would 
probably be due to the simple regeneration of the phagocyte army, 
or to extracts which, unsuspectedly, accompanied the supposedly in- 
tact leucocytes introduced. 


The infections in man which I and my coworkers have treated, 
through the courtesy and request of various physicians, have been 
those due to the meningococcus, pneumococcus, streptococcus, staphy- 
lococcus, and colon bacillus. 

There is not time, nor is this the place, to go into the histories of 
the individual cases. In connection with Dr. Zinsser in 1908 I 
published the results obtained in the treatment of a number of 
epidemic meningitis patients* and in a small number of patients 
Buffering from lobar pneumonia and pneumococcus infections, and to 
these articles I must refer anyone interested for details of these 
earlier tests. 8 


Meningococcus cases. — It may be of interest to state, however, that 
15 of the meningitis patients treated by us were under 15 years of 
age; of these, 3 died, leaving 80 per cent of recoveries with no 
sequelae. Of the patients over 15 years, there were 7, of whom 5 died. 
This result may have been due to the fact that several of these adult 
patients were in extremis when admitted to the hospital. In spite 
of this, under treatment some of the patients showed a marked im- 
provement, and did not die before 27, 7, 38, 11, and 25 days after 
treatment was begun. Of the children who were treated, but who 
died, 1 survived 79 days, 1, 62 days, and 1, a baby of 7 months, 12 
days, after treatment was instituted. 

It seems also of interest to note the fact that, in 7 cases in which 
treatment was begun subsequent to the seventh day of the disease, 
there was 100 per cent of recoveries without sequelae. Treatment was 
not begun in these cases until the elapse of 17, 20, 47, 41, 53, 39, and 
82 days after the first symptoms developed, and a reference to the 
histories would show that these patients were, as a rule, in grave 

Almost without exception there was an improvement in those symp- 
toms which, in this disease, depend largely on the central nervous sys- 
tems. Vomiting, delirium, stupor, and hypesthesia were usually 
diminished or entirety allayed after one or two administrations of 
quantities ranging from 5 to 20 cubic centimeters. 

Marked reduction in the temperature following injections was no- 
ticeable in many of the cases. In some of these cases, however, the 
diminution of the fever was a temporary phenomenon, limited to the 
24 or 48 hours immediately following the injection, a fact which also 
argues strongly for the idea of poison neutralization. 

The actual percentage of recoveries among these patients was about 
64 per cent. If 70 or 75 per cent be accepted as the usual death rate, 
and the basis for determining the value of the serum treatment of 
meningitis, then the fact that 64 per cent of our patients recovered 
would seem to indicate some curative value in the extract. And if this 
is true, it also indicates that if the antimeningitis sera are really 
toxin neutralizing, or contain the same antibodies as the leucocyte ex- 
tract, then these sera should be efficacious when administered sub- 
cutaneously, which is not the fact. I am inclined to believe that a 
combination of these treatments, immune serum given subdurally and 
leucocyte extract subcutaneously, might lead to more favorable re- 
sults than the use of either separately. 

Lobar pneumonia. — The total number of lobar pneumonia cases 
treated by us personally with leucocyte extract of which w T e have satis- 
factory records are 53. Out of this number 3 ended fatally, a mortal- 
ity of 5.6 per cent. Two of the fatal infections were in alcoholic 
patients. While this is of course not such an extended series as might 


be desired upon which to base* definite conclusions of the efficiency of 
the treatment, nevertheless the low mortality shown is encouraging, 
especially as the majority of the cases were severe, our aid not being 
asked until the patient was in an exceedingly unsatisfactory state. 
To those observing the course of the disease under this treatment, the 
most obvious effects of the extract were an almost immediate improve- 
ment in the feeling of well being of the patient, while, in the ob- 
jective symptoms, the improved quality of the circulation and reduc- 
tion of pulse rate, with a disappearance of cyanosis, usually accom- 
panied by an immediate drop in temperature, were noted ; some cases 
ending by an abrupt and early crisis, others coming to normal by a 
more gradual lysis. The spreading of the lesion was usually halted, 
and convalescence was usually rapid and uninterrupted. A striking 
effect of the treatment is the early disappearance of the distressing 
cough, which improvement has been especially apparent to the pa- 
tients themselves. As to the blo*od pictures, it has been noticed that in 
patients growing progressively worse with a falling leucocytosis. 
that the leucocytes increased almost immediately, giving in a few 
hours a more normal and favorable blood picture. A general con- 
clusion from a study of all our cases is that the disease is rendered 
largely benign, and in patients treated early, the length of the disease 
is markedly shortened. In cases treated late, the crisis usually comes 
on in a few hours. 

The doses usually given have been from 20 to 60 cubic centimeters, 
and repeated every four hours until marked improvement occurs. 

Such occurrences as these, backed by the conclusive evidence of the 
animal experiments, would certainly seem to warrant an extended and 
careful study of the influence of this agent on pneumococcus infec- 
tions in man, and make us hopeful that many an otherwise fatal ill- 
ness may become comparatively benign under its influence. This hope 
is strengthened by evidence gathered from the study of infection due 
to the streptococcus, so closely related to the pneumococcus in many 

Streptococcus infections. — Erysipelas is a streptococcus infection 
which is an ideal infection to study, as the chief lesion is in plain 
view, and there is usually a sharp temperature reaction in the infec- 
tion. Moreover, a well-marked train of symptoms, which are un- 
doubtedly toxic in origin, is generally present, and as the leucocyte 
extract seems to act primarily, at least in combating toxemia, we have 
therefore a comparatively reliable means at our disposal of judging 
of its effects, both on the lesion and systemic symptoms. 

The mortality rate of erysipelas is given as about 10 per cent in 
adults; in children, as 75 per cent; and in infants under 1 year as 
almoel LOO per cent. Erysipelas, therefore, can not be counted as a 
light infection. 



Nevertheless, the opinion does not seem to be rare that erysipelas is 
a trivial, self-limiting disease that can safely be left to run its course 
under local treatment. 

During the last two years, however, we ourselves have had reports 
of 12 fatal cases of erysipelas occurring not in patients of the ex- 
tremes of age but for the most part in strong healthy adults. The 
need for more efficient therapeutic measures is therefore evident. 

The series of erysipelas infections treated with the leucocyte extract 
comprises 126 cases of all types and grades of severity. The 
majority of infections were secondary to operative measures and 
might be classed as surgical erysipelas, while the others were of the 
so-called idiopathic form, as the origin could not be traced to any 
contributing trauma or known lesion. As regards severity^ they were 
nearly all severe infections, and the great majority of them were of 
the most severe type that occurs. This was due to the fact that we 
were usually not consulted until the ordinary remedies had been 
tried, by which time the infection was well established and the 
systemic symptoms marked. Thus, with the exception of a few, the 
lesion had been present for a time, varying from several days to two 
weeks. Such cases, therefore, probably offer as fair a test of the 
value of a therapeutic agent as could be desired. 

The results obtained have been so uniformly beneficial, constant, 
and marked that judging from them it would seem that in this disease 
we can almost prognosticate the results following the use of leucocyte 

In every case there was a marked reaction following its use, which 
in most cases was shown by a fall in temperature and a rapid im- 
provement in the general condition. 

In an average case of erysipelas, one of moderate severity, the 
constitutional symptoms, due to the absorption of the toxins, are well 
marked — headache, nausea, vomiting, delirium, sometimes active but 
usually of a low muttering type, and a sense of extreme depression. 
The local subjective symptoms are also marked and are very annoy- 
ing, the heat, burning, and itching. In practically all the cases the 
symptoms disappeared within a few hours following the first injec- 
tion of the extract; the headache, nausea, and vomiting disappeared, 
the mind became perfectly clear, and from a low, depressed, appre- 
hensive state the patient passed into a state of comparative comfort, 
free from anxiety. The effect on the temperature varied with the 
class of patient and with the time that had elapsed between the onset 
of the lesions and the beginning of the treatment — in those treated 
early, within 24 or 48 hours of the onset, there was a sharp fall in the 
temperature curve, and the disease ended practically by crisis, the 
accompanying symptoms disappeared, and the rash ceased to spread. 


In the cases treated later in the course of the disease there was usually 
not such a marked effect on the temperature, but the change in the 
general condition was just as marked and the course of the disease 
cut short. Locally, in all cases, whether treated early or late, the 
burning and aching pain disappeared in a few hours. Subjectively 
the patient was soon in an entirely different state. 

As regards the effect of the extract on the local lesions, there was 
generally some further spreading, but the character of the lesion 
changed. The bright vivid crimson rash, usually seen in an other- 
wise healthy patient, soon ceased to spread and faded. The dull 
purplish rash, seen in the deeper erysipelas infections or in the 
asthenic type of patient, soon gave way to the bright crimson form, 
which change we take to be evidence of increased resistance, and this 
in turn faded away gradually. In the latter class of patients, where 
a severe infection was present with the corresponding systemic 
symptoms and a low temperature curve, a moderate rise of tempera- 
ture at times occurred after the infection. This we looked upon as a 
favorable sign and as an evidence of increased resistance. 

The duration of an average case of erysipelas, under the routine 
measures of treatment, is about 10 to 14 days. In our series of cases 
the average duration, whether treatment with the extract was insti- 
tuted early or late, was 3-1 days after treatment was begun. 

In practically all cases following the use of the leucocyte ex- 
tract, had it not been for the mere physical presence of the diseased 
focus, the patient would have been considered well. 

The extract took the place of all stimulation, and patients suffering 
from the most severe infections have been kept entirely comfortable 
by the use of the extract alone, with a pulse rate usually not rising 
above 90, thus showing the saving of the human economy. 

With post-operative or surgical erysipelas one point is worthy of 
special notice. Most of these infections were complications of opera- 
tions on the eye, ear, nose, and throat. The point to be noted is that 
under this treatment the healing instead of being delayed, as usual, 
was hastened and was complete in a much shorter time than in an 
uncomplicated case. We refer especially to mastoid wounds. This 
is directly contrary to the usual experience with such wounds, as very 
often, following erj^sipelas, it is necessary to do a second operation 
to clean out the flabby unhealthy granulations. The same would hold 
true with operative measures on other parts of the body. 

The foregoing general description of the effects of leucocyte extract 
on erysipelas represents not only our own conclusions from the 
observation of patients so treated but is based largely upon conclu- 
sions drawn by the physicians and surgeons under whose care many 
of these patients were. 




For purposes of analysis little would be gained by giving histories 
of the patients treated. The histories fall into more or less distinct 
groups which we simply summarize in the following table : 

Statistical analysis of erysipelas cases. 

Age of patient. 

Infants (up to 1 year).. . 
Children (1 to 15 years). 
Adults (15 to 50 years). . 
Over 50 years 


No. of 



Time of treatment. 1 

/Early 5 

\Late 7 

/Early 3 

\Late 7 

(Early 36 

\Late 58 

/Early 4 

\Late 6 

(Early 48 

\Late 78 

duration of 











Termination of 

Recovery. Death 




* Early = Treatment begun within 3 days of appearance of lesion; Late= 
days after appearance of lesion. 


■ Treatment begun later than 3 

Total number of cases treated, 126; recovered 121, mortality 3.96 per cent. 

General average duration of treatment, 3.18 days. 

Number of recoveries under 1 year old, 8 out of 12. 

Per cent of recoveries under 1 year old, 66.6 per cent. 

General mortality rate, 3.96 per cent (all cases). 

Mortality among patients over 1 year, 0.87 per cent; recoveries, 99.13 per cent. 

In addition to these cases, Dr. Adrian Lambert, in his wards at 
Bellevue Hospital, has treated about 50 cases of erysipelas by this 
method, with extract supplied by us. While the history of these 
cases will be published in detail by Dr. Lambert, his conclusions are 
as follows: 

Leucocyte extract will abort infections which are treated within the first 48 

It will ameliorate the course of older infections and may abruptly terminate 
them ; the longer the infection has existed, the less likely is the latter to take 
place, but it tends to shorten the course of the disease. 

The toxic symptoms — delirium, headache, nausea, and vomiting — are modified 
and relieved ; local pain is lessened. 

The rash does not disappear immediately, but is apt to be localized. 

The spreading intractable lesions of the back and body are apparently affected 
as readily as those occurring on the face and head. 

Pus formation is aborted, and sequelae are rare, if they occur at all. About 
50 per cent of babies under 1 year of age have recovered from the erysipelas. 

Our conclusions, as has been stated, are practically the same as 
these, although we show even a more favorable outcome of the treat- 
ment in babies under 1 year of age. 

Staphylococcus infections. — Local acute and chronic staphylococcus 
infections respond almost immediately to treatment with the extract. 


and furunculosis of intractable type is halted and apparently cured. 
Dr. Zinsser has treated 11 patients who had staphylococcus infection. 
In these, after treatment was begun, surgical interference was always 
unnecessary, and Dr. Dwyer has also treated a large number of 
patients with various staphylococcus infections with uniformly favor- 
able results. 

1 The method of obtaining these substances as used in animal experiments 
and the treatment of human subjects is at present as follows : Rabbits, of 1,500 
grams weight or heavier, receive intrapleural injections of aleuronat. This is 
prepared by making a 3 per cent solution of starch in meat-extract broth, 
without heating, and adding to this, after the starch has gone into thorough 
emulsion, 5 per cent of powdered aleuronat. This is thoroughly mixed, boiled 
for five minutes, and filled into sterile potato tubes, 20 cubic centimeters into 
each tube. Final sterilization is done, preferably in an autoclave. The rabbit 
injections are carried out by injecting 10 cubic centimeters into each pleural 
cavity in the intercostal spaces at the level of the end of the sternum, in the 
anterior axillary line, great care being exerted to avoid puncturing the lungs. 
The rabbits are left for 24 hours, at the end of which time a copious and very 
cellular exudate will have accumulated in the pleural cavities. After killing 
the animals, this is removed by opening the anterior chest wall under rigid 
precautions of sterility, and pipetting the exudate into sterile centrifuge tubes. 
Immediate ceiitrifugalization, before clotting can take place, then permits the 
decanting of the supernatant fluid. To the leucocytic sediment is then added 
about 2 cubic centimeters of sterile distilled water, and the emulsion is thor- 
oughly beaten up with a stiff bent spatula. Smears are now made on slides, 
stained by Jenner's blood stain, and examined for possible bacterial contami- 
nation. It is well also to take cultures. Sterile distilled water is then added 
to each tube, about 10 volumes to 1 volume of sediment, and the tubes are 
set away in the incubator for seven or eight hours. At the end of this time 
the sterility is again controlled as above, and further extraction in the refrig- 
erator continued until the extract is used. So far as at present determined, the 
preparation remains active indefinitely. Before use the preparation is thor- 
oughly shaken to disseminate the sediment, which is then drawn into the 
syringe and injected subcutaneously along with the fluid into the animal or 

2 Hiss : Jour. Med. Research, 1908, XIX, 323. See this article for details of 
these and the following experiments on animals. 

8 Jour. Med. Research, 1908, xvi. 


Dr. E. Libman, New York: In cases of furunculosis I have seen 
better results from the use of the leucocyte extract than from that of 
vaccines. I would like to ask Dr. Hiss whether he has seen any 
anaphylactic reactions, and how often. I observed in one case an 
urticarial rash with temperature elevation after the fourth injection, 
the latter l)eing given within a few days after the first. The 
symptoms rapidly subsided. 





Dr. D. L. Haeris, Bacteriologist to Hospital Department, St. Louis, Mo. 

The object of this paper is to present the results of an attempt to 
produce a rapid antirabic immunity by direct immunization of the 
brain cells. 

The method devised by Pasteur for the prevention of hydrophobia 
limited this work to large and well-equipped laboratories and required 
the patient to undergo treatment for a period of three weeks or more. 
Several modifications have been adopted from time to time, which 
have made the work of preparing the material less onerous and the 
treatment more available to the public, especially to those patients 
living at a distance from such a laboratory. In all antirabic institutes, 
whatever modification may have been adopted in the preparation 
of the material, the treatment consists in a number of injections into 
the abdominal wall. The result of this is an indirect immunization 
of the brain cells against the infective agent. In spite of all treat- 
ment, however, a small number of the patients die before immunity 
can be established. 

During the past year I have described a method for preserving the 
virus used in antirabic immunization. This, in brief, consists in 
freezing with carbon dioxide snow the brain and cord of a rabbit 
infected with the disease and drying these in a vacuum at a tem- 
perature of —10° C. Material prepared in this manner, and kept 
free from moisture in an ice box (10° C.) loses its infectivity so 
slowly that after a preservation of 40 weeks one-tenth of a milli- 
gram, when injected subdurally, will produce paresis in a rabbit in 
7 days; in other words, after 8 months of desiccation, its infectivity 
is equal to that of Pasteur's 2-day cord. 

In testing the desiccated material from time to time to determine 
the effect of time, temperature, and light on the rate of loss of in- 
fectivity, I observed that some rabbits which had received subdurally 
a quantity of the virus slightly less than the minimal infective dose 
developed an appreciable and determinable immunity against sub- 
sequent subdural inoculations. 

Ten rabbits were immunized in this manner, and the degree of 
immunity thus acquired was ascertained by one or more later tests. 
Of these ten, six resisted an injection sufficient to kill untreated con- 
trols. One did not develop the disease after an injection of twice 
the minimal infective dose. One survived the injection of 100 mini- 
mal infective doses. Two died on the fifteenth and seventeenth days, 
respectively, after the injection of twice the minimal infective dose. 

Of seven rabbits that survived the first test, four were inoculated 
later with 10 minimal infective doses of street virus. Two survived 


and two died on the eighteenth day. Table No. 1 x gives the results 
of these experiments in detail. All injections were made under the 
dura after trephining. 

Tests made in one lot of material which had been kept for some 
months at room temperature in daylight showed this to be non- 
infective, and it was observed that the rabbit inoculated with this 
material had also acquired an immunity. (Table I. R. No. 9.) 

Following this a number of rabbits were given larger quantities of 
noninfective material intraspinally. 

In these experiments, the details of which will be seen in Table 
No. 2, 2 rabbits 1, 2, and 3 were injected intraspinally with material 
which had been kept in an ice box for 66 days, and then in the light 
at room temperature for 219 days. Rabbits 4, 5, and 6 were injected 
with material that had been kept in a north window, room tempera- 
ture, for 11 months. When these six were injected the technic of 
making the spinal puncture was undeveloped, and it was suspected 
at the time that the needle had not entered the spinal canal of rab- 
bits Nos. 1 and 4. Their susceptibility to a later inoculation of four 
minimal infective doses showed this suspicion to have been well 
founded. Rabbits Nos. 7 to 19 were injected with material which 
had been in the dark at room temperature for eight months. Rab- 
bits 20 to 23 were injected with material which had been kept in 
the presence of P 2 5 , which, it has been demonstrated, causes a rela- 
tively rapid destruction of virulence. 

Rabbits No. 24 to 27 were injected with desiccated street virus 
whose infectivity had been destroyed by placing it in direct sunlight 
(west window) for three weeks. The material was obtained from 
a case of rabies in a woman and was the brain of a rabbit, first pas- 
sage. It had been desiccated five months. It will be seen that 
three of these rabbits were not immune to 10 minimal infective doses 
14 days after the injection, but that the fourth resisted a similar 
inoculation 28 days later. The action of direct sunlight may have 
been a factor in lessening the immunizing capacity of the material. 
It is of interest to note that street virus may be used for immuniza- 
tion by this method. 

Rabbit No. 28 was injected subdurally (trephine) with material 
which had been kept in an ice box for 7 months, and in one of the 
laboratory rooms in daylight for 39 days. Rabbit No. 29 is the 
same as No. 7, and, after surviving this test, was reinoculated 44 
days later. 

These experiments show that the brain of a rabbit may be directly 
immunized by a single intraspinal injection of nonvirulent material 
to such a degree that two weeks later the animal successfully with- 
stand ;: subdural injection of 10 to 20 times an otherwise fatal dose. 
The immunity is acquired so rapidly that the intraspinal injection 


of 5 milligrams or more will* protect against a simultaneous inocula- 
tion of a minimal infective dose injected subdurally (trephine). 

Similar experiments were made on dogs, as follows: Three dogs 
were injected by lumbar puncture with 50 milligrams of noninfective 
material, and 16 days later were inoculated under the dura with -^ 
milligram of the medulla of a rabid dog (desiccated). 

In another series one dog was given 10 milligrams of a non- 
infective desiccated brain; two dogs 20 milligrams; two dogs 40 
milligrams; and the five were inoculated eight days later with -fa 
milligram of desiccated street virus. Two other dogs were injected 
with 50 and 25 milligrams intraspinally, and at the same time were 
inoculated under the dura with ^ milligram of desiccated street 
virus. Two dogs were used as controls. The estimated amount of 
infective virus received by each of these 12 dogs was five times the 
infective dose for rabbits. 

One of the control dogs developed furious rabies on the fourteenth 
day. The other control became emaciated 5 weeks later; on the 
forty-fourth day refused food, and died on the forty-sixth day after 
a paralysis which developed a few hours earlier. The autopsy did 
not reveal any cause of. death and Negri bodies were not found in 
the brain. One of the two dogs, inoculated and immunized at the 
same time, became extremely emaciated 5 weeks later, developed 
paralysis on the thirty-sixth day, and died on the thirty-eighth day. 
The remainder of the immunized dogs have shown no recognizable 
injury following the inoculation. 

The above experiments seem to show that it is comparatively easy 
to immunize rabbits against rabies by a single intraspinal injection 
of noninfective desiccated " virus," and that the resulting immunity 
is acquired with surprising rapidity. The test on the dogs is some- 
what unsatisfactory, because the amount inoculated was too small 
to produce a definite and early outbreak of the disease in both con- 
trol animals. It does appear, however, that the intraspinal injec- 
tion is not followed by any ill results. 

Whether or not fixed virus may be rendered noninfective by 
methods other than the one I have employed without at the same time 
lessening its immunizing value is a question which offers an oppor- 
tunity for further investigation. It appears that the material whose 
infectivity was destroyed by P 2 5 , and by direct sunlight, did not 
liave as great an immunizing value as the material which had been 
allowed to die more slowly. 

If further investigations show that the intraspinal injections of 
this material are harmless to animals, and that immunity is regu- 
larly and rapidly conferred, we may be in possession of a means of 
saving some of those patients who have received severe injuries 
about the face and who now succumb in spite of the treatment em- 


ployed at the present time. Another advantage of this method is 
that the immunizing property of the material I have used is not 
affected by age, and it may be stored in quantity and kept anywhere 
for immediate use. 

1 Table No. 1. 


of first 
tion (in 

Time of 

(in mini- 
mal in- 

Time of 


(in mini- 
mal infec- 
tive doses 
of street 


No. 1 





1 1 






Died fifteenth day. 
Died seventeenth day. 

No. 2 

No. 3 

No. 4 











No. 5 


No. 6 


No. 7 


No. 8 


No. 9 


No. 10 


i Milligram. 

2 Table No. 2. 


Amount injected. 

Time of inoculation. 

Amount in 
doses of 

fixed virus. 


No. 1... 
No. 2... 

20 milligrams of fixed virus 


10 days later 

























No. 3... 

do do 


No. 4... 




No. 5... 




No. 6... 




No. 7... 

25 milligrams of fixed virus 

Same time 


No. 8... 

20 milligrams of fixed virus 



No. 9... 

5 milligrams of fixed virus 

4 davs later 


No. 10. . 

20 milligrams of fixed virus 



No. 11.. 

5 milligrams of fixed virus 

6 days later 


No. 12.. 

10 milligrams of fixed virus 



No. 13.. 

15 milligrams of fixed virus 



No. 14 . 

5 milligrams of fixed virus 

8 days later 


No. 15 

10 milligrams of fixed virus 



No. 16.. 



No. 17.. 

15 milligrams of fixed virus 



No. 18.. 

20 milligrams of fixed virus 

14 days later 


No. 19.. 


15 days later 


No. 20. . 

20 milligrams of fixed virus (P2O&) 


Same time 


No. 21.. 

14 days later 


No. 22.. 

do !... 



No. 23. . 




No. 24.. 

12 milligrams of street virus 

Same time 


14 days later 


No. 26. 

20 milligrams of street virus 



No. 27.. 

12 milligrams of street virus 

28 days later 


No. 28.. 

20 milligrams of fixed virus 

11 days later 


No. 29. . 

25 milligrams of fixed virus 

44 days later 



Amer. Journ. Physiol. XXIV, p. 325. 

Journ. Infect. Diseases, Vol. X, No. 3, 1912, p. 369. 

Annates de l'Inst. Pasteur, XXVI, p. 732. 



Anna W. Williams, Division of Laboratories; Director Wm. H. Park, Health 

Department, City of New York. 

For the past two years the New York City Health Department has 
been studying trachoma and allied conditions and it plans to continue 
these studies for about two years more. The full report will 
contain details of the work. So far in our investigations we may 
summarize our results briefly under seven heads as follows: 

I. Hemoglobinophilic bacilli are found in cases of " trachoma " 
practically coincidently with " Prowazek (trachoma) in- 
II. These bacilli show the same cycle of development as that of 
the " Prowazek inclusions." 
III. These bacilli so far can not be differentiated from B. of Koeh- 

Weehs or B. influenzae. 
IV. Clinically, cases beginning as acute contagious conjunctivitis 
(Koch- Weeks infection) may pass into the condition known 
as trachoma. 
V. The above facts lead to the hypothesis that " trachoma " is 
caused by infection with one or more of the group of hemo- 
globinophilic bacilli, producing primarily an acute inflamma- 
tion, and, secondarily, in susceptible cases, a subacute and 
chronic productive inflammation. 
VI. Acting on this hypothesis for the past year and a half the acute 
contagious conjunctivitis cases as well as those of " trachoma 
and allies " have been closely followed and treated in schools 
and homes. Now, there are practically no new cases of 
" typical trachoma." 
VII. An opportunity to test further this hypothesis is afforded by 
the establishment of special mixed classes in schools for the 
isolation, study, and treatment of these cases. 
There are just a few points which I wish to emphasize under each 
of these heads. 


1. In all fresh untreated cases of papillary trachoma, where the 
Prowazek (trachoma) inclusions were present, we found the hemo- 
globinophilic bacilli. In many cases which were old when first 
seen, and in a number of recovering cases we found neither the 
Prowazek inclusions nor the hemoglobinophilic bacillus. In the 
rest of these cases the inclusions and bacilli were irregularly present, 
the inclusions generally in small numbers. 

2. Frequency of isolation. — Other investigators have isolated mem- 
bers of this group of bacilli from trachoma, but not so regularly. 


Our success is probably due to our special technic. This technic has 
already been published. 1 

The bacilli often may not be isolated because they are so readily 
overgrown by other microorganisms, especially by the staphylococcus 
pyogenes, which, as you know, is found not seldom in inflammations 
of the conjunctiva. 

We hoped to obtain some help in isolating our bacillus from these 
cases from Churchman's (1912) gentian-violet-medium but have been 
disappointed, because we found that while this medium inhibited 
the Gram positive organisms in pure cultures it did not appreciably 
inhibit them in mixed cultures with the blood medium used by us. 


Under head II we wish to emphasize the resemblance between our 
bacilli and the trachoma inclusions. 

1. These bacilli in young cultures stain as the initial bodies of 
Lindner. Later they form tiny metachromatic granules, passing 
through a cycle similar to that described for the trachoma inclusions. 

We have carried through a number of different varieties of bac- 
ateria found in diseased conjunctivae, in order to find out whether 
other varieties show a similar cycle, and we have found that while 
most of them show a few metachromatic granules in later cultures, 
only one variety shows them to the extent seen in our hemoglobino- 
philic bacilli. It is interesting to note, considering Hertzog's hy- 
pothesis that the inclusions are altered gonococci, and considering 
the work done on the finding of trachoma inclusions in ophthalmia 
neonatorum and in vaginal and urethral cells, that the other variety 
is the gonococcus. We have found in certain cases of gonorrheal 
ophthalmia all stages of inclusions from gonococcal forms up to 
metachromatic granular forms, and we haye found certain minute 
differences between this series of changes (corresponding with those 
found in pure cultures of the gonococci) and the series of changes 
seen in the inclusions of chronic conjunctivitis cases in which we have 
found the hemoglobinophilic bacilli, where again we find a complete 
series of changes in the inclusions, from definite bacillus forms up to 
metachromatic granular groups; these, also, as I have said, corre- 
sponding with the changes observed in pure cultures. 

The chief differences so far observed in the cycle of these two 
species of bacteria is that, in the gonococcus, the groups are more 
dense and the metachromatic granules are finally smaller than in the 
hemoglobinophilic bacilli. 

From these observations, it seems to me quite probable that the 
gonococci, as well as the hemoglobinophilic bacilli, produce so-called 
" Chalmydozoal, Prowazek, or Trachoma inclusions." 


Of course, there may be cases of mixed infection. If these are 
facts, they explain all of the recent contradictory findings in gonor- 
rhoea!, as well as in papillary, conjunctivitis (trachoma) cases. This 
hypothesis also explains Dr. Noguchi's (1911) findings in his series 
of gonorrhoeal ophthalmias showing the Prowazek inclusions. 

In regard to the etiology of trachoma, however, we must still con- 
sider two important series of investigations — one, animal experi- 
ments, and the other filtration experiments. 

A number of investigators have reported the production of 
trachoma in the conjunctiva of Pavian monkeys, after suitable in- 
oculations. Unfortunately, we have had, so far, only a few Macacus 
species with which to work, and in one out of four we have gotten a 
moderate subacute conjunctivitis, without inclusions, after inocula- 
tions with our bacilli from which we recovered the bacillus. 

In regard to filtration, it has been claimed that the virus of 
trachoma is filterable. The results of these investigations are still 
under discussion. I can only say that we are just starting experi- 
ments on the filterability of our small bacilli, especially with cultures 
at different stages, in order to determine the passage of the tiny 
granules; for, without doubt, as with other bacilli, some of these 
granules at a certain stage of their growth represent the last living 
element of the bacilli. With sufficient dilution arid pressure they 
may with comparative ease pass at least some of the coarser filters. 


Under the third heading I wish to call attention to the following 
points : 

1. Our bacilli with the influenza bacilli, as well as all of the many 
strains of Koch- Weeks bacilli with which we have worked, are so 
far, strict hemoglobinophiles in pure cultures. 

Those observers who have obtained successive growth of the Koch- 
Weeks bacillus on serum, must have used serum which contained a 
small amount of hemoglobin. These bacilli will grow in serum 
containing 1 : 1000 blood, which means a quantity of hemoglobin that 
can not be detected by ordinary tests. The spectroscope does not 
discover this amount. We have found only Adler's benzidene test 

2. All the other tests we have used to differentiate these strains, 
such as complement deviation, simple and acid agglutination, etc., 
have, so far, shown no clear-cut differences between them. There is 
no doubt, however, reasoning from the findings in other similar bac- 
terial groups, that there are, at least, distinct varieties among them, 
and that there are variations in pathogenicity which could account 
for the different clinical findings. 

66692— vol 2. pt 1—13 6 



Under the fourth heading we consider the clinical study of our 

The relationship between acute contagious conjunctivitis and tra- 
choma has often been discussed. But very few observers have had, or 
have taken the opportunity (judging from published reports) to follow 
cases beginning as acute contagious conjunctivities through a series 
of attacks until a subacute and chronic condition is reached with all 
of the earmarks of trachoma. We have, apparently, been able to 
do this in a certain number of cases, and obtained, apparently, good 
histories in a certain number of other cases, not only in New York 
City, but in the Kentucky Mountains where trachoma is in evidence. 
This has materially aided us in reaching our conclusion, that, clinic- 
ally, cases of trachoma are intimately related to acute contagious 


Our hypothesis in regard to the etiology of trachoma, which is 
given under the fifth heading, requires much study before it can be 
proved; but, considering the results stated in the sixth heading, 
practically, we are justified in using it as a working hypothesis. 
And, in the immediate future, with the establishment of the special 
mixed classes the Board of Education has allowed us, we hope that 
while we are attempting to cure and stamp out the disease, we may 
at the same time add material to the evidence as to the nature of 
trachoma, at least in our New York City school children. 

1 Significance of the group of hemophilic bacilli in conjunctivitis, especially 
in that of trachoma. Proceedings of N. Y. Path. soc. an. 10-1912; New York 
Med. J., Mar. 16, 1912. 


K. Landsteiner fragt an, ob irgend ein Unterschied zwischen den 
von Williams beobachteten Bacillen und dem von Miiller als Ursache 
des Trachoms vermutheten haemoglobinophilen Bacillus besteht. 



A. Weber, Dr. med.. Geb. Reg. Rat, Direktor der bakteriologiscbeu Abteilung 
des Kaiserlicben Gesundheitsnmtes, Berlin. 

Auf dem XIV. Internationalen Kongress fiir Hygiene und Demo- 
graphie, Berlin 1907, erstatteten Babes und Lojfler Referate iiber die 
Bazillen der Typhusgruppe, in denen sie den dankenswerten Versuch 
machten, die grosse Anzahl der hierhergehorigen, verschiedenartigen 
Bakterien in besondere, umschriebene Gruppen und Untergruppen 
einzuteilen, und so auf diesem noch etwas verworren liegenden 
Gebiete durch Aufstellung einer bestimmten Klassifikation bessere 
Uebersicht und Ordnung zu schaft'en. Lofjier hat dabei alle in Be- 
tracht kommenden, von ihm mit dem Sammelnamen Tj^phaceen 
bezeichneten Bakterienarten nach ihrem kulturellen Verhalten gegen- 
iiber seinen beiden Griinlosungen in die 3 Hauptgruppen der Typha- 
ceae, der Josarceae und der Coleae zusammengefasst und bei diesen 
wieder nach dem serologischen Verhalten wie bezgl. der Pathogenitat 
verschiedene Untergruppen aufgestellt. 

Im Anschluss an die beiden Referate von Babes und Lofjier wurde 
dann von Sektion I des Kongresses f olgender Beschluss gef asst : 

" Um die Erkenntniss der iiberaus wichtigen Bakterien der Typha- 
ceen zu fordern, sollen eingehende vergleichende Untersuchungen der 
samtlichen zu den Bakterien der Typhusgruppe gehorenden Orga- 
nismen vorgenommen werden." 

Mit diesen Untersuchungen wurden 7 Institute betraut, und 
bestimmt, dass iiber die Resultate auf dem nachsten internationalen 
Hygienekongress berichtet werden sollte. 

Ich habe die Ehre, Ihnen iiber die im Kaiserlich Deutschen Reichs- 
gesundheitsamt in Berlin unter Leitung meines Amtsvorgiingers 
Geheimen Regierungsrat Professor Dr. Uhlenhuth ausgefiihrten, 
insbesendere die Bakterien der Paratyphusgruppe betreffenden 
Untersuchen Mitteilung zu machen. 

Nach diesen Untersuchungen lassen sich in der Tat die verschie- 
denen der Typhusgruppe zuzurechnenden Bakterienarten auf Grund 
ihres Wachstums in den erwahnten Loffler'schen Nahrmedien im 
allgemeinen nach 3 grossen Gruppen abteilen, wobei allerdings das 
Verhalten eines Stammes gegeniiber den beiden Griinlosungen immer 
nur einen gewissen Anhaltspunkt iiber seine Stellung gibt, wahrend 




zu seiner naheren Bestimmung die Heranziehung weiterer Nahrboden 
notwendig ist. Ebenso gibt eine erweiterte kulturelle Priifung erst 
Aufschluss iiber die zahlreichen zwischen den einzelnen Gruppen 
stehenden Uebergangsvarietaten. 

Im allgemeinen werden jetzt wohl ziemlich iibereinstimmend fur 
die genauere kulturelle Differentialdiagnose der der Typhusgruppe' 
zuzurechnenden Bakterien ausser den beiden Lofflerlosungen haupt- 
sachlich noch 9 andere Nahrmedien, namlich Milch, Lackmusmolke, 
die Nahrlosungen Barsiekow I u. II, die Nahrlosung nach Hetsch, 
Neutralrotagar, Orceinagar, sowie Traubenzucker- und Milchzucker- 
bouillon verwertet. Eine moglichst einheitliche und an alien in 
Betracht kommenden Stellen gleichmassig durchgefuhrte Benutzung 
solcher bestimmten Nahrsubstrate konnte fiir die Erkenntnis der 
kulturellen Verhaltnisse bei den hierhergehorigen Bakterien wie fur 
die Erzielung ubereinstimmender Resultate nur forderlich sein. 

Bei den im Kaiserlichen Gesundheitsamt durchgefiihrten Unter- 
suchungen sind die genannten Nahrboden jedenfalls regelmassig 
herangezogen und die besten Erfahrungen damit gemacht worden, so 
dass dieses Vorgehen in jeder Hinsicht nur bestens empfohlen werden 
kann. Die nachstehende Tabelle enthalt eine Zusammenstellung des 
Wachs turns der hauptsachlichsten Vertreter der der Typhusgruppe 
zuzurechnenden Bakterien auf den angefiihrten Nahrboden. 

Barsiekow I. 

Loffler I. 

Loffler II. 




B. typhi. 

Gerinnung, iiber 


Keine Ge- 

Unverandert bzw. 

Rotung und 

dem Gerinsel 


leichte Rotung, 


klare, griine 

keine Triibung. 

Fliissigkeit, kei- 

ne Schaumbil- 

B . dysenterise 


Keine Ge- 

Leichte Rfttung, 




keine Triibung. 

B. aysenterise 

Zuweilen Gerin- 


Keine Ge- 

Leichte Rotung, 





keine Triibung. 

B. paratyphi A. 



Keine Ge- 

Rotung and Trii- 

Rotung und 

schaumige Ge- 




rinnung, Fliis- 
sigkeit triibe. 
Gerinnung, iiber 


B. typhi suis 


Keine Ge- 

Unverandert bzw. 



dem Gerinsel 
klare, griine Fliis- 
sigkeit, keine 
Gerinnung, iiber 


leicht gerotet, 
keine wesent- 
liche Triibung. 

B. Voldagsen. 


Keine Ge- 

Leicht gerotet, 

Rotung und 

dem Gerinsel 


keine erhebliche 


klare,|grune Fliis- 


sigkeit, keine 


B. paratyphi B. 


Lelchte Tru- 

Keine Ge- 

Zunachst gerotet 

R6tung und 

schaumige Ge- 



alsdarm Blau- 


rinnung, Fliis- 


sigkeit triibe. 

B. enteritidis 

Leichte Trii- 

Keine Ge- 

Zunachst gerotet 

Rotung und 


schaumige Ge- 
rinnung, Fliis- 
sigkeit triibe. 



alsdann Blau- 


B. coli. 


S c h m u t z i g- 


Rotung und Trii- 

Rotung und 

schaumi^o Ge- 




rinnung, Fliis- 


sigkeit triibe. 





Barsiekow II. 






losung nach 




B. typhi. 


Leichte Ro- 

Keine Gas- 

Keine Gas- 




tung, Gerin- 





nung, keine 

B. dysenteriae 



Keine Gas- 

Keine Gas- 

Un veran- 









B. dysenteriae 

Un veran- 

Rotung, keine 

Keine Gas- 

Keine Gas- 

U n v e r ii n- 









B. paratyphi A. 


Rotung, keine 


Keine Gas- 





bung, Gas- 

bung und 

fa i 1 d ung, 





B. typhi suis 



Zumeist kei- 

Keine Gas- 






ne Gasbil- 


kend zu- 
meist un- 
z u weilen 
wie vor- 


B. Voldagsen. 




Keine Gas- 


G e r i n g e 





bung, Gas- 
b i 1 d ung, 
F 1 u ores- 


B. paratyphi B. 

Un veran- 

R6tung, Ge- 

G a s bil- 

Keine Gas- 




rinnung , 




bung, Gas- 
fa i 1 d ung, 
F 1 u o res- 

bung und 
G a s bil- 

B. enteritidis 

Un veran- 

Rotung, Ge- 


Keine Gas- 





rinnung , 




bung, Gas- 
b i 1 d u ng, 
F 1 u o res- 

bung und 
G a s bil.- 

B. coli. 

Rotung und 

R5tung, Ge- 






rinnung , 




bung, Gas- 
bi ldung, 
F 1 u o res- 

bung und 
Gas bil- 

Es ist dabei allerdings zu erwahnen, dass die Tabelle nur eine 
schematische Uebersicht iiber die Wachstumsverhaltnisse der einzel- 
nen Bakterienstamme gibt, da bei Priifung einer grossen Anzahl von 
Kulturen derselben Art, sich doch mitunter mehr oder weniger stark 
ausgesprochene Schwankungen bezgl. der Intensitat des chemischen 
Reaktionsausfalles auf dem einen oder dem anderen Nahrboden gel- 
tend machen konnen, die zum Teil allerdings auch von der Art der 
verwendeten Zuckerpraparate (Ditthom) abhangen. Im allgemeinen 
darf man aber doch das in der Tabelle angegebene Verhalten als 
das fur die einzelnen Bakterienarten charakteristische bezeichnen. 

Vergleicht man an der Hand dieser tabellarischen Zusammenstel- 
lung das Wachstum der verschiedenen Bakterienarten, so lassen sich 
auch hier nach dem kulturellen Verhalten auf den genannten Nahr- 
boden 3 Hauptgruppen abtrennen, namlich : 

A. Die Typhusgruppe in engerem Sinne, der hinsichtlich der kul- 
turellen Eigenschaften auch die verschiedenen Ruhrerreger nahe- 
stehen ; 

B. Die G^uppe des Bazillus Paratyphi B, des Bac. enteritidis 
Gartner und der Kulturell gleichen Baktericuarten ; 

C. Die Gruppe der Colibakterien. 


Dazwischen finden sich zahlreiche verschiedene Uebergangsva- 
rietaten, welche sich in kultureller Hinsicht mehr der einen oder der 
anderen Gruppe naheren, und von denen in der Tabelle ausser dem 
zwischen der Typhusgruppe und der Gruppe des Paratyphus B 
stehenden Bazillus Paratyphi A zwei von Gldsser und Dammann 
aus Schweinen isolierte und als Erreger einer besonderen bazillaren 
Form der Schweinepest angesprochene Stamme, namlich der Bazil- 
lus typhi suis Glasser und der Bazillus suipestifer Voldagsen auf- 
gef iihrt sind. Auf diese beiden Bakterienarten wird bei Besprechung 
der Paratyphusgruppe noeh des Naheren zuriickzukommen sein. 

Der Gruppe B, mit welcher sich hauptsachlich die weiteren Aus- 
fuhrungen befassen sollen, gehoren nun ausser dem eigentlichen Ba- 
zillus Paratyphi B Schottmuller und den bei den Gruppenerkran- 
kungen in Breslau, Meirelbeck, Diisseldorf, Sirault, Aertryck, Neun- 
kirchen, Greifswald u. s. w. isolierten Paratyphus B gleichen Stam- 
men, der Bazillus typhi murium, der Bazillus der Psittacose, der 
Bazillus suipestifer und, wie erwahnt, ausserdem der Bazillus en- 
teritidis Gartner, die bei den Epidemien von Moorseele, Gent, Kum- 
fleth, Haustedt, Brugge gefundenen, ihm gleichen Bakterien, sowie 
die als Eattenschadlinge bekannten, von Danysz, Dunbar, Issat- 
schenko u. a. bei Rattenepizootien gezuchteten Kulturen an. Eben- 
falls ihr zuzurechnen sind ferner die bei den Fleischvergiftungen 
in Lassan und Barth gewonnenen Kulturen, der Bazillus Paratyphi 
C. ( Uhlenhuth, Hubener) sowie die weiteren von zahlreichen Autoren 
(Titze, Weichel, Schmidt, Muller, Sobemheim, Seligmann, Jahobitz 
u. Kayser, Rimpau, Haendel u. Gildemeister, Messerschmidt u. a.) 
gefundenen Stamme, welche sich kulturell ebenfalls vollkommen wie 
der Bazillus Paratyphi B und der Bazillus enteritidis Gartner ver- 
halten, aber zu diesen in serologischer Hinsicht keine Beziehung 

Die Gruppe umfasst also im Wesentlichen die Stamme, welche 
man friiher mit verschiedenen Sammelnamen wie Hog-Cholera-, Sal- 
monella-, Flugge-Kaensche Gruppe und in neuerer Zeit meist unter 
der Bezeichnung Paratyphusgruppe zusammengefasst hat. Nicht 
verfehlen mochte ich an dieser Stelle darauf hinzuweisen, dass unser 
sehr verehrter Vorsitzender, Herr Professor Theobald Smith der 
erste war, der im Jahre 1894, noch vor Entdeckung der spezifischen 
Fleischvergiftungsbakterien die verwandtschaftlichen Beziehungen 
des Hogcholerabazillus zu andern Bakterien auf Grund morpholo- 
gischer und biologischer Merkmale festzustellen versuchte. Er war 
es, der die Hogcholera- oder Salmonellagruppe aufstellte, in die er 
ausser dem Bazillus suipestifer den Bazillus typhi murium, den Ba- 
zillus enteritidis Gartner und einen aus Abortus seiner Stute 
gezuchteten Bazillus rechnete. x Vgl. hiezu auch die in neuester Zeit 
erschienene Arbeit von de Jong, Uber einen Bacillus der Paratyphus 


B Enteritisgruppe als Ursache eines seuchenhaften Abortus der 
Stute. Centralbl. f. Bakteriologie, Abt I, Orig. Bd. 67, Heft. 3, 8. 


Allerdings diirfte es sich auch unseres Erachtens entsprechend der 
neuerdings von Soberheim aufgestellten Forderung empfehlen, diese 
Sammelnamen in erster Linie nur auf die Stiimme, welche sich nicht 
nur kulturell, sondern auch serologisch dem Bazillus Paratyphi B 
Schottmiiller gleich verhalten, zu beschranken, und nicht ohne 
weiteres auch auf die in ihrem serologischen Verhalten von den 
Paratyphusbazillen verschiedenen Kulturen, wie zum Beispiel die 
Stamme der Gartnergruppe auszudehnen, da es sich in beiden Fallen 
zwar um nahe verwandte, aber doch im allgemeinen einheitlich fiir 
sich abgrenzbare Bakterienarten hahdelt, wenn gleich sich bei ihnen, 
wie neuere Untersuchungen (Sobemheim u. Seligmann, Lentz, 
Rimpau, Haendel u. Gildemeister, BarthZein u. a.) gezeight haben, in 
dieser Hinsicht auch in ihrem serologischen Verhalten auffallende 
Schwankungen und eigenartige Verschiebungen geltend machen 

Trotz dieser spater noch zu besprechenden Veriinderlichkeiten wird 
aber doch daran festzuhalten sein, die Paratyphus- und Giirtnerbak- 
terien als besondere mit Hilfe der Immunitatsreaktionen differenzier- 
bare Arten anzusehen, wie dies zuerst von Uhlenhuth festgestellt 
worden ist. In morphologischer und kultureller Hinsicht lassen sich 
allerdings bei ihnen nach den bisherigen Untersuchungen keine kon- 
stanten, deutlich ausgesprochenen Unterschiede feststellen. Die von 
Babes erwiihnte Verschiedenheit in der Begeisselung des Paratyphus 
B- und des Gartnerbazillus ist nicht so deutlich ausgesprochen, dass 
sie fiir eine Differenzierung verwertet werden konnte, ebenso sind die 
von Babes erwahnten kulturellen Unterschiede, wonach die Giirtner- 
bazillen Neutralrot und Orcein energischer verfiirben wie die Para- 
typhusbakterien nicht so gleichmassig und durchgreifend, dass da- 
nach eine Trennung vorgenommen werden konnte. Auch die von 
einzelnen Autoren (Savage, Schern u. a.) auf besonderen Nahrboden 
beobachteten Differenzen finden sich nicht konstant. 

Dagegen scheinen in anderer Hinsicht vielleicht doch durchgreifen- 
dere kulturelle Unterschiede bei beiden Gruppen zu bestehen. Nach 
von Barthlein im Kaiserlichen Gesundheitsamt durchgefiihrten 
Untersuchungen lassen sich niimlich anscheinend bei alien Bak- 
terienarten unter bestimmten Bedingungen eigenartige, plotzlich 
einsetzende Abspaltungsvorgiinge feststellen, welche wir als Muta- 
tionsvorgiinge aufzufassen geneigt sind, und die in der Weise in 
Erscheinung treten, dass auf der gewohnlichen Agarplatte dieselbe 
Bakterienart gleichzeitig in verschiedenen Kolonieformen wiichst, 
welche sich jeweils wieder aus morphologisch differenten Bakterien 


zusammensetzen. Die mutierten Kolonieformen zeigen nun bei den 
einzelnen Bakterienarten im allgemeinen — auf die genaueren Einzel- 
heiten kann im Rahmen dieses Referates nicht naher eingegangen 
werden, es sei vielmehr verwiesen auf die in Band 40 der Arbeiten 
aus dem Kaiserlichen Gesundheitsamt erschienene Arbeit von 
Barthlein — ein charakteristisches Aussehen, so dass in manchen 
Fallen schon aus der Koloniebildung in gewissem Sinne ein Schluss 
auf die Zugehorigkeit einer Kultur zu einer bestimmten Bak- 
terienart gezogen werden kann. 

Die mutierenden Gartnerstamme wachsen nun auf der Agarplatte 
regelmassig auch in fur sie ganz charakteristischen, kleinen, 
gelbweissen, bei durchfallendem Licht stark perlmutterartig irisieren- 
den Kolonien, wahrend von den Bakterien der Paratyphusgruppe 
derartige Formen nicht gebildet werden. Nur der Bacus der Pspit- 
tacose macht eine Ausnahme, auch bei ihm entwickeln sich bei der 
Mutation dem Kolonientyp der Gartnerstamme entsprechende Kolo- 

Von dieser Ausnahme abgesehen scheint hier aber ein bemerkens- 
werter Unterschied in dem Verhalten der Stamme der Paratyphus- 
und Gartnergruppe wenigstens nach den bisherigen Beobachtungen 
zu bestehen. 

Wie liegen nun die Dinge bei gesonderter Betrachtung der der 
Gartner- und Paratyphusgruppe in engerem Sinne zuzurechnenden 
Bakterienarten ? 

Wenn wir uns zunachst der Paratyphusgruppe zuwenden, so hat 
man auch hier zunachst geglaubt, durch kulturelle Unterschiede den 
Bac. Paratyphi B Schottmuller von den bei Fleischvergiftungen 
gefundenen Paratyphus B-gieichen Stammen und den tierpathogenen 
Arten abtrennen zu konnen. Die Beobachtung von Babes, wonach 
die Letzteren und die Fleischvergiftungsstiimme Malachitgriin 
starker aufhellen wie die eigentlichen menschlichen Paratyphus- 
kulturen ist zwar nicht selten zutreffend, gestattet aber keineswegs 
eine durchgreifende Scheidung. Ebenso hat sich die Feststellung 
von v. Drigalski sowie von Fischer, dass sich frisch isolierte Para- 
typhus B Stamme des Menschen auf der Blauplatte durch die Bildung 
besonderer Kolonien mit deutlicher Randumwallung und eingesun- 
kenem Zentrum auszeichnen, bei spateren Untersuchungen {Kutscher 
u. Meinicke, Trautm,ann u. a.) nicht als konstantes Differenzierungs- 
merkmal verwerten lassen. 

Auch die interessanten Befunde R. M tillers, wonach es bei den 
Kolonien frisch aus dem Menschen isolierter Paratyphnsstamme zur 
Bildung eines eigenartigen Schleimwalles und auf Raffinoseagar zur 
Eotstehung kleiner, den Kolonien anfsitzender Knotchen kommt, 
wahrend die anderen Stamme, die Mausetyphus- und dieSchweine- 
pestkulturen nur knopflose Kolonien entwickeln, sind noch nicht bezgl. 


ihrer Konstanz so sicher gestellt, dass schon jetzt ein bestimmtes 
Urteil iiber den differentialdiagnostischen Wert dieser Krscheinungen 
abgegeben werden kann. Bei den Untersuchungen Barthlema iiber 
die auf der Agarplatte zu beobachtenden Mutationsvorgange haben 
sich jedenfalls nach den bisherigen Beobachtungen keine durchgrei- 
fenden Unterschiede bei den verschiedenen Stiimmen der Paraty- 
pliusgruppe feststellen lassen, und man kann sich nach allem nur 
dahin aussprechen, dass auf Grund kultureller Merkmale eine Schei- 
dung des Bac. Paratyphi B von den Fleischvergiftungsstiimmen und 
den tierpathogenen Arten der Gruppe auch heute nicht moglich ist. 
Aehnlich liegen auch die Dinge bezgl. der Moglichkeit einer Difl'eren- 
zierung mit Hilfe der biologischen Immunitatsreaktionen. Schon 
die ersten Untersuchungen von Trautmann, Uhlenhuth, Kutscher 
u. Meinicke, Bock u. a. haben gezeigt, dass auch bei diesen Priifungen 
eine Trennung zwischen dem Paratyphus B Bazillus, den entspre- 
chenden Fleischvergiftern und den tierpathogenen Arten nicht mog- 
lich ist. Mit Hilfe des Castellanischen Absattigungsversuchs wollen 
allerdings Nishino zwischen dem Paratyphus B Bazillus und dem 
Mausetyphusbazillus, sowie Bainbridge, Savage u. a. zwischen den 
Ersteren und dem Bac. suipestifer Unterschiede gefunden haben. 
Auch kann in der Tat schon nach fruheren von Bock im Kaiserlichen 
Gesundheitsamt ausgefuhrten Untersuchungen diese Methode bei 
Verwendung bestimmter Stamme derartige Ergebnisse liefern, sie 
versagt aber nach den Feststellungen von Uhlenhuth u. Hiibener, 
sobald die Versuche an einer sehr grossen Zahl von Kulturen vor- 
genommen werden. 

Entsprechend haben auch die in nejierer Zeit mit der Komplement- 
bindung (Altmann, Ballner u. Reibmayer) und mittelst der Anaphy- 
laxie (Lieverato) ausgefuhrten Differenzierungsveruche zu negativen 
Ergebnissen gefiihrt. 

Trotzdem wir so nicht in der Lage sind, mit Hilfe der bisher an- 
gewandten Methoden die einzelnen Bakterienarten der Paratyphus- 
gruppe sicher zu unterscheiden, so konnen wir sie andererseits aber 
auch noch nicht ohne weiteres alle, namentlich auch die verschieden 
tierpathogenen Stamme, als eine mit dem menschlichen Paratyphus 
B Bazillus vollkommen einheitliche Art auffassen, da sich doch bei 
ihnen zum Teil im pathogenen Verhalten, zum Teil auch in serolo- 
gischer Hinsicht eigenartige, wenn auch nicht durchgreifende Ab- 
weichungen geltend machen, welche noch weiterer Klarung bediirfen 
und zu einer gewissen Vorsicht bezgl. der Beurteilung in dieser 
Hinsicht mahnen. Urspriinglich hatte man dazu geneigt, als Grund- 
lage fiir eine Einteilung und Abtrennung der einzelnen Arten ihr 
pathogenes Verhalten zu verwerten, es hat sich dann aber ergeben, 
dass auch auf dieser Basis eine scharfe Trennung nicht durchzu- 
fiihren ist. Durch die Versuche zahlreicher Autoren (Kutscher- 


Meinicke, Shibayama, Uhlenhuth-Hubener u. a.) wurde vielmehr 
festgestellt, dass grundsatzliche, durchgreifende Unterschiede bei 
den verschiedenen Arten bezgl. ihrer Pathogenitat fiir kleinere Ver- 
suchstiere sowie fiir imsere Schlachttiere nicht bestehen, insbeson- 
dere hat Schmitt den Nachweis erbracht, dass auch menschliche Pa- 
ratyphusstamme eine Infektion der Schlachttiere bewirken konnen. 
Ebenso hat es sich ferner gezeigt, dass auch den tierpathogenen Arten 
eine gewisse Pathogenitat fiir den Menschen zukommt. So ist nicht 
nur die Moglichkeit einer Infektion des Menschen durch Mausety- 
phuskulturen und Rattenschadlinge, sondern auch durch Schweine- 
pestbazillen sowie durch den Bazillus der Psittacose durch die Beob- 
achtungen von Trommsdorff, Fleischanderl, Meyer, Shibayama, 
Ungar, Babes und Busila, Handson und Williams, Silberschmidt, 
Rochi und Tiberti, v. Slooten, Dewes u. a. Autoren erwiesen worden. 

Vom Deutschen Reich und von Preussen sind im Jahre 1905, vom 
Oesterreichischen Ministerium des Innern im Jahre 1910 Verhal- 
tungsmassregeln zur Verhiitung von Gesundheitsschadigungen durch 
Beschaftigung mit Mausetyphusbazillen bekannt gegeben worden 
(vergl. Veroffentlichungen des Kaiserlichen Gesundheitsamtes 1905 
S. 332 und S. 683, sowie 1910 S. 591). 

Hier moge auch das Resultat eines nicht veroffentlichten Selbstver- 
suches, den Reg. Rat. Dr. Beck im Jahre 1903 im Kaiserlichen 
Gesundheitsamt angestellt hat, Erwahnung finden. 

Beck nahm 2 ccm einer 48 stiindigen bei Zimmertemperatur in Ma- 
germilch gewachsenen Reinkultur von Mausetyphusbazillen mit 100 
ccm lauwarmen Thees vermischt zu sich. Am folgenden Tage wurde 
of teres Gurren im Leibe verspurt ; am 3. und 4. Tage erf olgte geringer 
Durchfall mit 3-4 maliger schmerzloser Entleerung von diinnfliis- 
sigem gallig gefarbtem Stuhl. Das Allgemeinbefinden war in keiner 
Weise verandert, vor allem bestand keine Temperatursteigerung, der 
Appetit war unverandert gut. Im Stuhlgang waren am 3. Tage 
nach der Aufnahme reichliche Mengen von Mausetyphusbacillen 
nachweisbar. Im Ausstrich auf Agar-Agar entwickelte sich eine 
Reinkultur dieser Stabchen. Diese konnten noch am 10. Tage nach 
Beginn des Versuchs durch ein besonderes Anreicherungsverfahren 
im Stuhl festgestellt werden, waren aber vom 15. Tage ab verschwun- 
den. Eine an dem selben Tage angestellte Agglutinationsprobe mit 
dem Serum der Versuchsperson ergab noch bei einer Verdiinnung 
von 1 : 300 eine deutliche Agglutination. 

Andererseits ist aber auch zuzugeben, dass in gewisser Hinsicht 
eine besondere Pathogenitat fiir bestimmte Tierarten bei den einzelnen 
Untergruppen doch starker hervortritt. Es kann sich bei dieser 
Tatsache zwar nur um eine allmahlich erworbene Anpassungser- 
schoinung handeln, sie konnte aber unter Umstanden doch auch in 


bestimmten, uns bisher noch unbekannten Differenzen bei den betr. 
Arten begriindet sein. In dieser Hinsicht ist eine neuerdings von 
Haendel u. Gildemeister mitgeteilte Beobachtung vielleicht von In- 
teresse, wonach agglutinierende Sera, welche mit den bereits erwahn- 
ten von Gldsser u. Dammann aus Schweinen isolierten Paratyphus- 
ahnlichen Stammen gewonnen waren, verschiedenevonihnengepriifte 
Pestiferstiimme ebenfalls bis zur Titergrenze agglutinierten, Para- 
typhus B Stamme dagegen nicht oder doch nicht in nennenswerter 
Weise beeinflussten. Diese Beobachtung war besonders auffallend, 
weil der Bazillus typhi suis und der Dammannsche Bazillus sich 
kulturell nicht nur untereinander, sondern auch deutlich ausge- 
sprochen von dem Wachstum der Pestifer- und Paratyphusstamme 
unterscheiden. Der Bazillus Gliisser lasst Lackmusmolke, die 
Hetsch'sche Losung, sowie Neutralrot und Orcein unverandert, 
wahrend der Bazillus Voldagsen Lackmusmolke und den Hetsch?- 
schen Nahrboden ebenfalls unverandert lasst, oder die ersteren nur 
leicht rotet, dagegen Neutralrot und Orcein deutlich aufhellt. Auf 
Traubenzuckerbouillon zeigen die Kulturen insofern ein schwanken- 
des Verhalten, als beide hier bald Gasbildung bewirken bald nicht. 

Haendel u. Gildemeister konnten ihre Beobachtungen ferner noch 
dahin erganzen, dass auch Sera, welche sie mit von ihnen aus schweine- 
pestkranken Schweinen isolierten Paratyphus B gleichen, aber fur 
Paratyphus- und Gartnersera inagglutinablen Stammen hergestellt 
hatten, das gleiche Verhalten zeigten und ausschliesslich Glasser- 
und Voldogsen- Stamme und, wenn auch nur in geringerem Grade, 
Pestiferkulturen, nicht aber Paratyphus stamme agglutinierten. 
Diese Befunde sind an einem grossen Kulturmaterial von 
Teodoraseu weiter verfolgt und bestatigt worden. 1 Es hat 
danach den Anschein, als ob sich unter den Paratyphus B- und 
Pestiferstammen nach dem agglutinatorischen Verhalten gegenuber 
den betr. heterologen Seris 2 Gruppen abtrennen lassen, von denen 
die eine, welche sich meist aus von Schweinen und Schlachtwaren 
gewonnenen Kulturen zusammensetzt, hoher beeinflusst wird wie die 
andern, welche hauptsachlich aus von Menschen geziichteten Para- 
typhus B Stammen besteht. Allerdings kommen einzelne Ausnah- 
men vor, sodass bei einer derartigen Trennung nach dem aggluti- 
natorischen Verhalten gegenuber den heterologen Seris vereinzelte 
aus dem Menschen gewonnene Stamme der Pestifergruppe und 
umgekehrt einzelne aus Schweinen stammende Kulturen der Para- 
Typhus B Gruppe zuzurechnen sind. 

Es mussen aber auch hier erst die Ergebnisse noch weiterer Unter- 
suchungen abgewartet werden, ehe iiber den differentialdiagnostischen 
Wert dieser Erscheinung ein bestimmtes Urteil gefallt werden kann. 
Zu beriicksichtigen ist dabei, dass bei den Glasser- und Voldagsen- 
stammen und ebenso bei den Paratyphusgleichen aber fur Para- 


typhussera inagglutinablen Kulturen offenbar in dem agglutinato- 
rischen Verhalten auffallende Veranderungen auftreten konnen. 
Dammann und Stedefeder hatten urspriinglich angegeben, dass ihre 
Kulturen nicht durch Pestifersera beeinflusst wurden, und dass 
umgekehrt Voldagsensera auch Pestiferstamme nicht agglutinierten. 
Uhlenhuth, Haendel u. Gildemeister haben diese Angabe bestatigt, 
sie beobachteten aber, dass die Voldagsenstamme sich bei der Fort- 
ziichtung in ihrem Verhalten anderten, spater durch Pestifersera 
agglutiniert wurden und auch Sera erzeugten, welche Pestiferstamme 
gleichfalls beeinflussten. Gleichzeitig machten sich bei den betr. 
Kulturen auch Veranderungen im kulturellen Verhalten bemerkbar. 
Spater haben Haendel u. Gildemeister auch Voldagsenstamme gefun- 
den, welche sofort nach der Isolierung aus dem Schwein bereits von 
Pestiferseris agglutiniert wurden. Die betreffenden Stamme ver- 
halten sich demnach in kultureller und agglutinatorischer Hinsicht 
auffallend labil. Das gleiche gilt nun wenigstens bzgl. des aggluti- 
natorischen Verhaltens auch fur die Paratyphusgleichen aber 
urspriinglich fiir Paratyphussera unempfindlichen Stamme. Bei den 
unter der Leitung Vhlenhuths im Kaiserlichen Gesundheitsamt 
durchgefuhrten Untersuchungen liber Schweinepest sind eine grosse 
Anzahl derartiger Kulturen aus Schweinen isoliert und lange weiter 
verfolgt worden. Dabei hat es sich gezeigt, dass nicht selten solche 
Stamme in Laufe der Zeit spater doch durch Pestifer- oder Gartner - 
Sera agglutiniert wurden, wenn sie auch ihre agglutinatorische 
Sonderstellung zunachst ein Jahr oder noch langer behauptet hatten. 
Andere ebenso lange in Beobachtung stehende Kulturen dagegen 
sind fiir Paratyphus- und Gartner-Sera standig inagglutinabel 
geblieben, wurden aber zum Teil von Glasser und Voldagsenseris 

Ueber ganz ahnliche Schwankungen auch bei typhischen Paraty- 
phus B- und Gartnerstammen war schon vorher von Sobernheim, 
und Seligmann berichtet worden. Diese Autoren hatten die Beobach- 
tung gemacht, dass typische Paratyphusstamme ihre Agglutinierbar- 
keit mit Paratyphusseris allmahlich immer mehr einbiissten, und 
dafiir in immer zonehmendem Masse von Gartnerseris beeinflusst 
wurden, sodass sie schliesslich mit den ersteren so gut wie nicht mehr 
und nur noch mit den letzteren reagierten. Gleichzeitig machten 
sicl) bei den betr. Stammen auch kulturelle Veranderungen bemerk- 
bar, indern die Kulturen auf der Agarplatte ganz anders aussehende 
Kolonien bildeten wie zuvor. Dagegen hatten sie ihren Artcharak- 
ter als Paratyphusstamme insofern bewahrt, als mit ihnen her- 
gestellte Immunsera nur Paratyphusbakterien, nicht aber Giirtner- 
1< ult lire n agglutinierten. Noch auffallender waren die bei Giirtner- 
stammen festgestellten Veranderungen. Im Allgemeinen liegen 
zwar auch bei den Gartnerbakterien die Verhaltnisse iibnlich, wie sie 


vorstehend fiir die verschiedenartigen Bakterien der Paratyphus- 
gruppe geschildert wurden. Auch bei den einzelnen Bakterienarten 
der Gartnergruppe, den Rattenschiidlingen, den Kalberruhrstammen 
(Jensen, Uhlenhuth-Hubener, Titse-W eichel u. a.) und den von 
Menschen stammenden Kulturen ist eine scharfe, durchgreifende 
Trennung und Einteilung in bestimmt umschriebene Untergruppen 
auf Grund kultureller Differenzierungsmerkmale oder mit Hilfe 
der Immunitatsreaktionen nach den Untersuchungen von Uhlen- 
huth, Xylander, Steffenkagen, Schern, Titze, Weichel u. a. nicht 

Allerdings lassen sich anscheinend nach den Feststellungen von 
Sobe?mheim *und Seligmann auch unter den Gartnerstammen bei 
Benutzung bestimmter Sera in gewisser Hinsicht nach dem Ver- 
halten bei der Agglutination und Complementbindung 2 Untergrup- 
pen abtrennen, von denen die eine hauptsachlich Eattenschadlinge 
umfasst. Auch die von Beniasch mit der Saureagglutination 
erhaltenen Befunde weisen auf gewisse Differenzen hin. Die Ergeb- 
nisse sind aber doch nicht so scharf und eindeutig, dass sie zu einer 
vollstandigen Abtrennung der 2 Gruppen ausreichen, zumal eine 
grosse Anzahl anderer Sera beide Typen vollstandig gleichmassig 
beeinflussen. Dazu kommt, dass man nach den von Sdbemheim u. 
Seligmann erhobenen ausserordentlich auffallenden Befunden bei der 
Gartnergruppe mit einer noch viel starkeren Veranderlichkeit 
einzelner Stamme rechnen muss, als bei den Paratyphusbakterien. 

Sobernheim u. Seligmann konnten namlich aus 2 urspriinglich 
typischen Gartnerstammen, den Kulturen Rumfleth u. Haustedt 
eine ganze Reihe von Tochter- und Sonderstammen gewinnen, welche 
zum Teil nach ihrem serologischen und kulturellen Verhalten noch 
Beziehungen zur Gartnergruppe aufwiesen, zum Teil aber voll- 
standig andersartige Kulturen darstellten und sich leils dem Bac. 
Paratyphus A oder dem Coli mutabile ahnlich, teils vollkommen wie 
Typhusbazillen verhielten. Diese ausserordentlich auflallenden 
Beobachtungen konnen vorlaufig nur als solche vermerkt werden, sie 
bediirfen noch weiterer Kliirung, ehe eine bestimmte Beurteilung 
dieser Befunde moglich sein wird. Das Eine lasst sich allerdings 
schon heute mit Sicherheit sagen, dass sich unter den Stammen der 
Paratyphus- und noch mehr der Gartnergruppe Kulturen finden, bei 
welch en biologische Umwandlungen nachzuweisen sind, und die 
sowohl in ihrem kulturellen wie auch serologischen Verhalten 
ausserordentlich eigenartige und auffallende Schwankungen und 
Veranderungen zeigen konnen. 

Neben diesen zunachst hauptsachlich ein wissenschaftliches In- 
teresse beanspruchenden, bemerkenswerten Befunden iiber das 
biologische Verhalten der Paratyphus- und Gartnerbakterien haben 
die neueren Forschungen iiber diese Bakteriengruppe auch zu in 


praktischer Hinsicht wertvollen und namentlich fiir die Epide- 
miologic der durch diese Erreger bedingten Krankheiten wichtigen 
Ergebnissen gefiihrt. 

Bei den im Kaiserlichen Gesundheitsamt unter der Leitung Vhlen- 
huths durchgefiihrten Untersuchungen iiber die Schweinepest wurde 
die Tatsache festgestellt, dass im Darminhalt gesunder Schweine 
Bazillen vorkommen konnen, welche von echten Pestifer- und Paraty- 
phusbakterien nicht zu imterscheiden waxen. Auf Grund dieser 
Beobachtung haben Vhlenhuth und seine Mitarbeiter schon in ihrer 
ersten Arbeit iiber das Wesen der Schweinepest die Bedeutung dieser 
Feststellung fiir die Epidemiologie des Paratyphus und der Fleisch- 
vergiftungen hervorgehoben und darauf hingewiesen, dass nach 
diesen Befunden nicht nur ein gelegentliches Uebergehen dieser 
Bakterien auf die Schlachtprodukte des Schweines anzunehmen sei, 
sondern dass man wohl auch mit ihrem Vorkommen bei anderen 
Tieren und mit ihrer weiteren Verbreitung in der Aussenwelt durch 
die Excremente der Tiere zu rechnen habe. Vhlenhuth hat sofort 
nach dieser Richtung Versuche aufgenommen, welche die geausserte 
Vermutung vollauf bestatigten. Gemeinsam mit Hubener konnte er 
in verschiedenen Wurstproben, in den Ausscheidungen gesunder Men- 
schen, welche von solchen Wurstwaren genossen hatten, und in einigen 
Milchproben derartige Bakterien nachweisen. Vhlenhuth u. Hubener 
fandem, dass diese Bakterien ferner bei Fallen von Kalberruhr 
vorkommen und auch im Darminhalt gesunder Kalber festzustellen 
sind. Bei vergleichenden Untersuchungen einer grosseren Zahl als 
Erreger der Kalberruhr beschriebenen Stamme konnten sie zeigen, 
dass unter diesen der Jensen'sche Paracolibazillus sich wie der Bac. 
enteritidis Gartner, verschiedene andere Kulturen wie Paratyphus- 
stamme verhielten. Diese Ergebnisse sind durch die Untersuchungen 
von Titze u. Weichel, Langkau, Sehmitt, bestatigt worden. Auch 
sonst sind bei kranken Kalbern, Kiihen und anderen grosseren Tieren 
von zaldreichen Autoren wie L anger , Bugge, Junack, Ledschbor, 
Dieudonne, Schmitt, Zeller, Zwick u. Weichel, Fally, Riemer, Eden- 
huizen, Franke, Zwick u. a. Paratyphus- und Gartnerbazillen gleiche 
Bakterien gefunden worden. Ferner sind solche Bakterien nachge- 
wiesen bei Affen (Tromsdorff u. a.), bei Papageien (Eckersdorff, 
DreweSy Setter) bei Sperlingen (Ta/rtakowsky u. Saequepee) und bei 
Kanarienvogeln (PfeilerfAdam und Meder u. a.). Bei der Pseudo- 
tuberkulose des Meerschweinchens wurden sie von Neisser, Bohme 
und Eckersdorff, von Dieterlen und Bo finger festgestellt, nachdem 
schon vorher Theobald Smith, van Ermengem und Durham auf das 
Vorkommen zur Paratyphusgruppe gehoriger Mikroorganismen 
bei dieser Erkrankung des Meerschweinchens aufmerksam gemacht 
hatten. Sic wurden ausserdem gefunden bei Epizootien von Ratten 
und Maus< wie im Kot und im Organ ismus von gesunden Indi- 


viduen dieser Tierarten (Uhlenhuth, Xylander, Schern, Trautmann, 
Muhlens, Dahm und Fiirst, Zwich u. a.), ferner im Kot von Meer- 
schweinchen und Kaninchen {Morgan und Smallmann) im Darmin- 
halt von Giinsen (Ileusser), im Hundekot (Vallet u. Rimbaud) , end- 
lich im Darminhalt von Fliegen (Nicoll und Torrey). 

Von besonderer Bedeutung ist ihr Nachweis bei gesunden Schlacht- 
tieren, bei unverdorbenen Fleisch- und Wurstwaren und anderen 
Nahrungsmitteln. Ausser den schon erwahnten Befunden von 
Uhlenhuth und Hubener wurden sie von Grabert, E chert, Conradi, 
Trautmann, Seiffert, Schmidt, Sobernheim u. Seligmann, Rimpau, 
Buthmann, Rommeler und von anderen Autoren im Darminhalt, 
bezw. in den Organen von gesunden Schlachttieren oder in Schlacht- 
waren gefunden. 

Im Wasser und Eis sind sie ebenfalls Aerschiedentlich so von 
Forster, Sternberg, Gathgens, Georg Mayer, Conradi, Rommeler u. a. 
und in Milchproben von Hubener, Conradi, Klein und Georg Meyer 
nachgewiesen worden. In Uebereinstimmung mit diesen Befunden 
konnten audi in den Faeces gesunder Menschen, bei denen nach- 
weisbare Beziehungen mit Paratyphusf alien oder mit an Fleisch- 
vergiftung erkrankten Personen nicht nachzuweisen waren derartige 
Bakterien von Hubener und Viereck, Conradi, Kayser, Gathgens, 
Rimpau, Kilster Marmann u. a. aufgefunden werden. Dass bei 
diesen Befunden die Ausschiedung der mit Nahrungsmitteln 
aufgenommenen Bakterien in Betracht kam, konnte Conradi dadurch 
experimentell erweisen, dass er eine mehrkopfige Familie zum Genuss 
von derartige Bakterien enthaltendem rohem Hackfleisch veranlasste 
und darnach in den Stuhlgangen und in dem Blut der Frau die 
betreifenden Bakterien nachweisen konnte, ohne dass irgend eine 
Storung des Allgemeinbefindens bei einer der Personen zu beobachten 
gewesen ware. Conradi bezeichnet diese Art der Bakterienaus- 
scheidung als alimentare Ausscheidung. Im allgemeinen wahrt die 
Ausscheidung der Keime in solchen Fallen nur kurze Zeit, und die 
Anzahl der Bakterien ist gering. Allerdings liegen nun auch eine 
Reihe von Angaben von Seiffert, Trautmann, Amako, Aumann, 
Sobemhevm, Schmidt, Konig u. a. vor, wonach auch bei umfang- 
reichen Untersuchungen eiu solch verbreitetes Vorkommen dieser 
Bakterien im Darminhalt und den Organen der Schlachttiere, bei 
Schlachtwaren und anderen Nahrungsmitteln etc., sowie beim 
Menschen nicht festgestellt werden konnte. In England wird von 
Bainbridge und Brion die Existenz der gelegentlichen Ausscheider 
ganz in Abrede gestellt. Diese sich zum Teil widersprechenden 
Ergebnisse finden nach der Auffassung von Traut?nann, Sobernheim, 
Uhlenhuth und Hubener darin ihre Erkliirung, dass bei der Ver- 
breitung dieser Bakterien offenbar mit regionaren Verschiedenheiten 
und vielleicht auch zeitlichen Einfllissen zu rechnen ist. 


Sobemheim macht dabei zugleich darauf aufmerksam, dass auch 
bezgl. des Verlaufs der Paratyphuserkrankungen in gewisser Hin- 
sicht regionare Verschiedenheiten sich insofern bemerkbar machen, 
als in den nordlichen Teilen des Eeiches gegeniiber dem Siidwesten 
die Paratyphuserkrankungen hauptsaehlich als schwere Nahrungs- 
mittelvergiftungen oder als akute, choleraahnliche Anfalle, dagegen 
nur selten in der im Siidwesten des Eeiches iiberwiegender hervortre- 
tenden, mehr chronischen Typhus-ahnlichen Form des eigentlichen 
Paratyphus verlaufen. 

Auch bei den im Kaiserlichen Gesundheitsamt durchgefiihrten 
Untersuchungen liber Schweinepest ergaben sich Anhaltspunkte 
dafur, dass sich bei dieser durch ein filtrierbares Virus bedingten 
Krankheit ebenfalls bzgl. der Art der jeweils dabei auftretenden, 
dem Bazillus Pestifer oder dem Giirtnerbazillus gleichen oder 
ahnlichen Begleitbakterien anscheinend regionare Verschiedenheiten 
geltend machen konnen. Wie dem auch ist, jedenfalls ist daran 
nicht zu zweifeln, dass in verschiedenen Gegenden ohne nachweis- 
baren Zusammenhang mit Fleischvergiftungen oder Paratyphuser- 
krankungen bei Menschen und Tieren bei Schlachtprodukten und 
anderen Nahrungsmitteln u. s. f. nicht selten Bakterien gefunden 
worden sind, welche sich von den Erregern des Paratyphus, in 
manchen, allerdings bisher weniger zahlreichen Fallen von Gartner- 
bazillen nicht unterscheiden lassen. • 

Eine andere Frage ist es nun allerdings, wie die Pathogenitat dieser 
Bakterien fur den Menschen zu beurteilen ist, ob ihnen eine dem 
Paratyphus- oder Gartnerbazillus gleiche oder in Vergleich zu diesen 
geringere oder iiberhaupt keine Pathogenitat zukommt. Wie schon 
vorher ausgefiihrt worden ist, beweist der Umstand, dass wir in keiner 
Weise in der Lage sind, die betreffenden Bakterien von den echten 
Paratyphus- oder Gartnerbazillen zu unterscheiden, noch nicht mit 
Sicherheit, dass wir es bei ihnen mit Bakterien zu tun haben, die den 
genannten Infektionserregern vollkommen gleich zu stellen sind. Es 
vSpricht vielmehr manches dafur, dass ihnen im allgemeinen nur eine 
verhaltnismassig geringe Pathogenitat zukommt, da sonst bei ihrem 
haufigen Vorkommen die Zahl der Paratyphus- und Gartnerinfek- 
tionen eine weit hohere sein miisste, als sie nach alien Erfahrungen 
bisher beobachtet wurde. Andererseits haben wir aber auch keinerlei 
Anhaltspunkte, um mit Sicherheit ausschliessen zu konnen, dass nicht 
derartige Bakterien unter uns noch unbekannten Bedingungen fur 
den Menschen jederzeit pathogen zu werden vermogen. Es ist dabei 
besonders zu beriicksichtigen, dass auch bei den echten Paratyphus- 
und GiirtnerbaziJJen, wie wir wissen, ausserordentlich grosse Virulenz- 
unterschiede und Virulenzschwankungen vorkommen. Es ist hier 
ferner hinzuweisen auf die Beobachtungen von Uhlenhuth, Haendel 
und Stefjenhagen, sowie von Zwick und Weichel, wonach Ratten und 


Mause lange Zeit den Giirtnerbazillen gleiche Bakterien in vollig 
gesundem Zustande ausscheiden konnen, sofort aber an einer Gartner- 
infektion erkranken und zu Grunde gehen, sobald sie nach Impfung 
mit einem Tumor in ihrem Kriiftezustand zuriickgekommen oder un- 
ter ihnen nicht zusagende Fleischnahrung gesetzt werden. Auch 
konnen dann solche Tiere die Infektion auf andere gesunde Ratten 
und Mause iibertragen und zu ausgedehnten Epizootien Anlass geben. 
Es spricht nichts gegen die Annahme, dass auch beim Menschen durch 
derartige zuniichst scheinbar avirulente Bakterien unter Bedingun- 
gen, die wir nicht zu tibersehen im Stande sind, schwere Infektionen 
ausgelost werden konnen. Aus den bei der Erforschung der Schweine- 
pest gewonnenen Erfahrungen wissen wir, dass auch bei dieser 
Krankheit gerade Bakterien der Pestifer- und Giirtnergruppe sowie 
ihnen ahnliche Bakterienarten unter dem Einfluss des filtrierbaren 
Virus eine Virulenzsteigerung erfahren und sekundare bakterielle In- 
fektionen veranlassen konnen. Auch beim Menschen sind schon ent- 
sprechende Erfahrungen gemacht und z. B. unter dem Einfluss von 
Scharlach- (Bimpau) und Gelbfiebererkrankungen (Sanarelli u. a.) 
ein Virulentwerden derartiger Bakterien und nachtragliche Sekun- 
diirinfektionen beobachtet worden. 

Man wird deshalb nach allem an dem Vorkommen der betreffenden 
Bakterien doch nicht achtlos voriiber gehen diirfen, sondern die 
gegen Paratyphus und Fleischvergiftungen gerichteten Massnahmen 
auch auf sie ausdehnen miissen. Bei der im Siidwesten des Reiches 
eingerichteten organisierten Bekampfung des Typhus, welche dieser 
Infektionskrankheit gegeniiber zu so schonen und erfolgreichen Er- 
gebnissen gefiihrt hat, haben die bzgl. der Epidemiologic des Para- 
typhus und der Fleischvergiftungen gemachten Erfahrungen deut- 
lich gelehrt, dass hier fiir die Verbreitung und Uebertragung der 
Krankheitskeime die Verhaltnisse doch anders liegen und noch andere 
Wege in Betracht kommen, wie z. B. bei Typhus und Cholera, und 
dass ein Vorgehen, welches sich im wesentlichen und hauptsachlich 
nur gegen den infizierten Menschen richtet, bei der Bekampfung der 
durch Paratyphus- und Gartnerbakterien hervorgerufenen Kran- 
kheit nicht in gleicher Weise wie beim Typhus zum Ziele f iihrt. Der 
Kampf wird vielmehr gegen diese Krankheiten erfolgreich nur dur- 
chgefiihrt werden konnen, wenn clabei die bei ihnen vorliegenden 
besonderen Verhaltnisse darunter auch das Vorkommen dieser Bak- 
terien in der Aussenwelt beriicksichtigt werden. 

Im Rahmen dieses Referates war es selbstverstandlich nicht mog- 
lich, eine erschopfende Darstellung des Gebietes zu geben und alle 
Autoren, die dariiber gearbeitet haben, zu ihrem Rechte kommen zu 
lassen. In dieser Beziehung muss verwiesen werden auf die ausf uhr- 
lichen Darstellungen von Sacquepee, 2 Hubener, 3 und Sobernheim. 4 

66692— vol 2. PT 1—13 7 


Zum Schlusse mochte ich meine Ausfiirungen in folgende Satze 
zusammenfassen : 


I. Auf Grund des kulturellen Verhaltens auf den Loffier'schen 
Griinlosungen sowie auf den Differentialnahrboden Milch, Lackmus- 
molke, Neutralrotagar, Orceinagar, Traubenzucker- und Milchzuck- 
erbouillon, den Niihrlosungen nach Hetsch imd Barsiekow I. u. 
II. lassen sich die der Typhusgruppe zuzurechnenden Bakterien im 
allgemeinen nach 3 Hauptgruppen abtrennen : 

A. Die Typhusgruppe im engeren Sinne. 

B. Die Gruppe des Bazillus Paratyphi B, des Bazillus enteritidis 
Gartner und der ihnen kulturell gleichen Stamme. 

C. Die Gruppe der Colibakterien. 

II. Die Gruppe B zerfallt nach dem serologischen Verhalten in 3 
Untergruppen und zwar: 

Ba. Die Paratyphusgruppe, welcher ausser dem eigentlichen 
Bazillus Paratyphi B Schottmuller und den ihm bzgl. des kulturellen 
und serologischen Verhaltens gleichen Fleischvergifterstammen noch 
der Bazillus typhi murium, der Bazillus suipestifer und der Bazillus 
der Psittakose zugehoren. 

Bb. Die Gartnergruppe einschliesslich der verschiedenen Katten- 

Be. Die dem Bac. Paratyphi B und dem Bazillus enteritidis kul- 
turell vollkommen gleichen Stamme, welche aber durch die betreffen- 
den Sera nicht beeinflusst werden. 

Es erscheint zweckmassig die gebrauchlichen Sammelbezeich- 
nungen (Paratyphusgruppe, Salmonella, Flugge-Kaensche-, Hog- 
cholera-Gruppe) nur auf die Paratyphusgruppe im engeren Sinne 
-Untergruppe Ba-anzuwenden. 

III. Zwischen den einzelnen Angehorigen der Paratyphusgruppe 
(Ba) lessen sich weder bzgl. des kulturellen noch des serologischen 
Verhaltens, noch hinsichlich der Pathogenitat fiir Versuchstiere mit 
Hilfe der bisher angewandten Methoden grundsatzliche und durch- 
greifende Differenzen feststellen, trotzdem konnen aber nach den bis- 
herigen Erfahrungen die betreffenden Bakterien noch nicht mit 
Sicherheit als untereinander identisch angesehen werden. Das 
Gleiche gilt fiir die verschiedenen Angehorigen der Gartnergruppe. 

Die verschiedenen, dem Bac. Paratyphi B und dem Bazillus en- 
teritidis kulturell gleichen, aber fur die betreffenden Sera unempfind- 
lichen Stamme zeigen kein einheitliches serologisches Verhalten. 

IV. Bei den Paratyphus B- und Gartnerbazillen handelt es sich um 
gegenseitig zwar ebenfalls nahe verwandte, aber im allgemeinen doch 
einheitlich fiir sich abgrenzbare Bakterienarten. 

Henderson Smith.] Till. TYPHOID COLON CROUP. 99 

V. Unter den Stiimmen der Paratyphus- und der Giirtnergruppe, 
sowie unter den dem Bac. Paratyphi B und dem Bac. enteritidis 
Gartner kulturell gleichen aber fur deren Sera unempfindlichen Bak- 
terien finden sich Kulturen, welche ahnlich wie der Bac. Glasser und 
der Bac. Voldagsen sowohl in ihrem kulturellen wie auch serolo- 
gischen Verhalten Schwankungen und Veraridenmgen zeigen 

VI. Von Paratyphus- und Giirtnerbazillen nicht unterscheidbare 
Bakterien sind im Darminhalt normaler Individuen verschiedener 
Tierarten, in den Organen gesunder Schlachttiere, in Wurst- und 
Fleischwaren, bei anderen Nahrungsmitteln, in Eis und Wasser 
sowie in den Entleerungen gesunder Menschen gefunden worden, bei 
welchen Beziehungen mit Paratyphus und Fleischvergiftungen nicht 
nachzuweisen waren. Es ist deshalb mit einer Verbreitung derartiger 
Bakterien in der Aussenwelt zu rechnen, deren Art und Starke ans- 
cheinend von regionaren Verschiedenheiten und vielleicht auch von 
zeitlichen Einfliissen abhangig sein kann. 

1 In einer neuerdings erschienenen Arbeit (Zeitschr. f. Hyg., Bd. 73, S. 75) 
kommt Bernhardt zu entsprechenden Ergebnissen. 

2 Bull, de l'Institut Pasteur, T. V, 1907, und T. VIII, 1910. 

8 Htibener, Fleischvergiftungen und Paratyphusinfektionen, Jena (Gustav 
Fischer), 1910, sowie Vierteljahrsschr. f. gerichtliche Medicin u. offentliches 
Sanitiitswesen, Bd. XLIII, 1912, Nr. 15 und 16. 

4 Hygienische Bundschau, Jahrg. XXII, 1912, Nr. 15 und 16. 



Dr. J. Henderson Smith, Lister Institute, London. 


In the year 1906 M. Neisser recorded the occurrence of a coliform 
organism which, while primarily a nonfermenter of lactose, yet could 
give rise to a fermenting strain when grown on lactose agar. This 
organism was very carefully and thoroughly studied by Massini, who 
proved that the fermenting strain was not a contamination, but was 
really derived from the original nonfermenting organism and arose 
upon lactose agar as a variant with a new character which bred true. 
Since then numerous instances have been recorded by Burk, Jacob- 
son, Kevis, and others, and in particular by Twort and Reiner Miiller, 
of members of the colon-typhoid group which displayed a similar 
capacity of varying toward one or more of the carbohydrates, and the 
fact of bacterial variation in this direction is now beyond dispute. 
The important bearing which this fact may have upon the differen- 


tiation and identification of the pathogenic intestinal organisms is 
obvious, and for the last year or two W. J. Penf old has been carrying 
out in the Lister Institute a series of investigations on the subject. 
It is largely on his work that the following considerations are based. 

If a broth or peptone-water culture of a normal typhoid bacillus 
be plated on the surface of a dulcite-agar plate, to which neu- 
tral red has been added, the colonies which develop after incubation 
are all without exception colorless. They do not produce enough free 
acid to change the color of the neutral red, and it is reasonable to 
suppose that they are composed, at least for the most part, of individ- 
uals which do not ferment the alcohol. When we continue to observe 
such a dulcite-agar plate,, on which the colonies are discrete enough 
to allow of their free development, on a considerable number of the 
colonies papillae begin to appear, after a period which varies in 
different cases from 3 to 10 days. These papillae are small, very 
definite protuberances of characteristic appearance, somewhat irregu- 
lar in shape, and of variable size. Their number, per colony, as also 
the number of colonies which show them, varies considerably, but 
the number, both of papillae and of papillated colonies, usually in- 
creases as time goes on. Eventually a proportion of the papillae 
turn red. On these plate cultures of typhoid, then, the organisms, 
which at first failed entirely to show any signs of fermenting dulcite, 
now do so, but only in certain limited parts of the total growth. 

It might appear that what is occurring on the plates is that the 
organisms are turning to the dulcite as a source of food, having first 
exhausted the accessible supply of other constituents of the nutrient 
agar. In other words, that typhoid bacilli are capable of fermenting 
dulcite, but refuse to do so in the presence of other more appropriate 
nutriment. This is not the explanation of the late fermentation. If 
the organisms which compose such a papilla are plated out again upon 
dulcite agar, a number of the colonies which appear are red through- 
out, and these show no papillae. There is no longer an interval of 
several days, during which other food supply is being used up, but 
the fermentation begins early. The papilla then contains bacilli, 
which, unlike normal typhoid, are capable of attacking dulcite from 
the first. The papillated colony arose from a single organism of the 
original culture, and its progeny were at first, if not all, at all events 
preponderatingly nonfermenting. From among this progeny has 
arisen a strain, which now yields descendants preponderatingly fer- 
menting. This new character is at first unstable, and after a short 
period of growth on normal media, the fermenting strain will again 
give progeny all or nearly all nonfermenting. But continued selec- 
tion of colonies from dulcite agar or a few months' training on 
dulcite broth establishes the character, and a strain is obtained which 

Henderson Smith.] THE TYPHOID COLON GROUP. 101 

remains a dulcite fermenter, even after many months of cultivation 
in the absence of dulcite. 

The sequence of events is perhaps more easily followed on plates, 
but a similar process takes place in dulcite broth. All, or nearly all, 
normal typhoid strains eventually turn a dulcite broth acid, but the 
time taken to do so is very variable, varying, in Penfold's strains, 
from 5 to 15 days. This time can readily be reduced by continued 
culture in dulcite broth to 3 days, and, eventually, to 1 day. 
By following the changes which occur in litmus dulcite peptone 
water, inoculated with normal typhoid, Penfold has shown the 
sequence of events leading up to the eventual acidity of the medium. 
Multiplication at first occurs, just as in peptone water containing 
none of the alcohol, and reaches the maximum of some 200,000,000 
per 1 cubic centimeter, after which there is a slight decrease. During 
this period plating on dulcite agar shows that the organisms are non- 
fermenters. Then there develops a second rapid and very large 
increase in the number of organisms which may reach 600 to 1,000 
millions per 1 cubic centimeter. This is entirely due to the develop- 
ment of dulcite-fermenting organisms, and the medium turns acid. 
The nonfermenting individuals almost completely disappear, and it 
appears almost as if the two strains are antagonistic to one another. 
If, as occurs in one type of culture, the numbers do not show this 
second great increase, the nonfermenters remain permanently in the 
majority. Fermenting individuals appear, but do not gain the upper 
hand, and the medium does not turn the full deep red of marked 

So far as is known at present, growth on dulcite is the only means 
by which a dulcite fermenting strain can be obtained. This natu- 
rally suggests that the dulcite acts directly upon the individual ty- 
phoid bacillus in some specific manner, causing it to produce ferment- 
ing variants, which do not arise without this specific stimulus. This 
may eventually prove to be the correct view, but at present there is 
little to support it, and it is difficult to reconcile with some facts 
already known. If a nonfermenting individual be taken from a 
tube in which fermenting organisms have already arisen, it takes 
as long to produce a fermenting variant as an entirely untrained 
organism. It shows no indication of having been affected in any 
way by the dulcite, and there is nothing to suggest that it has been 
partially trained. The facts point rather to another interpretation 
w T hich is sufficient to account for them without the hypothesis of spe- 
cific alteration. It is enough to suppose that the normal typhoid 
bacillus, even growing on a broth medium without dulcite, tends to 
produce variants which have to a greater or less degree the power of 
fermenting the alcohol. 


On a nondulcite medium there is nothing to encourage this type 
as compared with others, and as on its first appearance it does not 
breed true and occurs in very small numbers, the variant disappears 
again. But if there is dulcite present such organisms as are able to 
attack it receive a stimulus to their multiplication which the non- 
fermenters do not receive, and increasing to a disproportionate ex- 
tent may eventually displace them entirely. The effect of the carbo- 
hydrate in the medium is to select one type of variant amongst those 
normally occurring rather than to induce the production of a quite 
new type. This increase of growth in the presence of an attackable 
carbohydrate is. as we have seen, what occurs in dulcite tubes when 
the fermenting variety appears, and it holds with other sugars also. 
A medium containing glucose, for example, supports and produces 
a larger population of typhoid than one which contains lactose or 
cane sugar, which the organism can not attack and in which the num- 
bers are approximately the same as when no sugar is present. If the 
typhoid has been previously " trained " to attack lactose, then the 
numbers exceed the normal and approach those of the dulcite variant 
or glucose populations. The development of a protuberant papilla 
of itself indicates a greater energy of growth on the part of its com- 
ponents than that of the rest of the colony. 

We have here, then, an instance of variability in the typhoid bacil- 
lus such that within a comparatively short time two races can be 
obtained differing from one another in the definite property of fer- 
menting dulcite. Several other variations in the properties of typhoid 
with regard to carbohydrates are known. Reiner Miiller has de- 
scribed the appearance of papiJlse on isodulcite, and Penfold, like 
him, has found this appearance of papilla? to be a constant character 
of typhoid. If isodulcite plates are made from these papillae, colonies 
are obtained which show no papilla?, and a race is obtained at once 
which breeds true and has lost the property of papilla formation 
upon isodulcite. An arabinose-fermenting strain is readily obtained, 
and strains are known which do and others which do not ferment 
glycerin. Special interest attaches to the lactose-fermenting variety 
produced by Twort. This organism was subsequently examined in 
detail by Penfold, and was found by him to be a genuine typhoid 
both in its lactose and nonlactose states, although it shows one or 
two slight divergencies from the perfectly typical B. typhosus. It 
took two years' constant growth on lactose before the variant could 
be obtained, and even now, after two years more on lactose, it docs 
not breed true, showing a strong tendency to throw out atavists and 
revert to its nonfennent ing state. After 18 months of training of a 
considerable number of strains on lactose media, Penfold has failed 
to produce another fermenting variety of B. typhosus, and it is evi- 
dent that it is only with great difficulty and after a very long growth 

Henderson Smith.] THE TYPHOID COLON GBOUP. 103 

on lactose that this particular variant can be produced from normal 
typhoid. Similar ill success has attended the attempt to produce 
variants by growth on a number of other media, such as adonite, 
erythrite, saccharose, amygdalin, salicin, and formates. 

It appears, then, that B. typhosus is an organism which can be 
made to alter its character with regard to many of the carbohydrates. 
But it appears, also, that the readiness with which variation occurs 
differs in different cases. On the one hand we have the isodulcite- 
papilla variant, which arises very rapidly with every strain, and has 
the new character fixed immediately. As an intermediate comes the 
dulcite variant, which can be obtained from most strains fairly 
easily, and can be fixed comparatively quickly. On the other hand, 
we have the lactose-fermenting variant, which can be obtained only 
after years of "training" and has not yet been made to breed true. 
It may be that even those characters which have not yet been found 
to vary are really only characters whose variants take exceptionally 
long to arise, and that there is no single carbohydrate character which 
may not vary at one time or another under particular conditions. 
However that may be, the readiness with which the variant appears 
and the ease with which it becomes fixed show in general a rough 
agreement, and the more disposed an organism is to produce a par- 
ticular variant the more readily is it disposed to take on the new char- 
acter permanently. 

It is probable that when other organisms have been examined in 
sufficient detail it will be found that they are like typhoid in this 
readiness to produce particular variants and reluctance to produce 
ofhers. Unfortunately the data on this point are still somewhat 
meagre. The occurrence of variants has been described for many 
members of the typhoid-colon group among the pathogenic as well 
as the so-called nonpathogenic organisms occurring in the gut. 
Thus Reiner Miiller has obtained papilla? with paratyphoid B on 
raffinose, and with Flexner's dysentery bacillus on isodulcite. Twort 
has induced the paratyphoids, and also Flexner and Shiga to ferment 
cane sugar, and Shiga has also been made to ferment lactose. Hiss 
so early as 1904 obtained a maltose-fermenting variant of bacillus Y, 
and other variations have been recorded. It is a pity that it is not 
always possible to ascertain from the published accounts how soon 
these alterations of character arose, nor whether the variants bred 
true, and in some cases the identity of the new strain with the old 
has not been very satisfactorily established. But it is clear that these 
variants show great differences in the readiness with which they arise. 
Massini's lactose-fermenting strain of B. colt mutabile, for example, 
arises at once and breeds true, while others require weeks or months 
of training on the particular sugar before a variant appears. More 
information is much needed on this point, for, so far as present 


knowledge goes, it seems likely that along this line is to be found the 
theoretical justification of the recognized practical value of the car- 
bohydrate tests. 

It has been asserted that the possibility of variation is sufficient to 
destroy the value of the carbohydrate tests as aids to the differentia- 
tion and identification of the organisms of this group. If it is pos- 
sible, so the argument runs, to make Shiga's dysentery bacillus fer- 
ment both lactose and cane sugar, we can not accept the absence of 
these properties as significant characteristics of the organism. If 
plates made from a suspected water or feces from a case of enteri- 
tis show only lactose- fermenting colonies, we can never be sure that 
these colonies, or some of them, are not really colonies of a typhoid 
variant. May not something of this kind be the real explanation of 
the extreme difficulty of isolating typhoid from water ? 

The difficulty must be admitted and the possibilit}^ recognized that 
so far as carbohydrate tests go, one organism may be convertible into 
another. We can, in fact, conceive the possibility of an organism 
with the sugar reactions of a B. coli and the agglutinating and other 
properties of a dysentery bacillus, including its pathogenicity. It 
may even be the case that in certain instances something of this sort 
does actualty occur in nature. 

Penfold has brought forward some evidence to show that, parallel 
to the main group of lactose-fermenting organisms in the intestine, 
there are corresponding groups of nonlactise-fermenting bacteria, 
occurring naturally in fair numbers, which belong to the mutabile 
class and are convertible into the fermenting t3 7 pes, and he considers 
that one group may arise from its corresponding group under nat- 
ural conditions. Even if this were proved, however, beyond dispute, 
it would not discredit the usefulness of the carbohydrate tests. It 
only shows us that there are certain organisms for which the lactose 
relation is unsuitable as a group character; it does not touch the 
possibility that there are other carbohydrates more suitable. These 
particular organisms of the mutabile group have a pronounced ten- 
dency to vary toward lactose, and this experience in the laboratory 
would lead us to anticipate the occurrence of such variants in nature. 
In a similar way, we know that typhoid has a» pronounced tendency 
to vary toward glycerin, and this laboratory experience would lead 
us to reject glycerin fermentation as a safe character of the typhoid 
group. 2 The dulcite-fermenting variety is less likely to arise nat- 
urally, but even this is a frequently occurring variation with a ten- 
dency to breed true. We should prefer to take, as a type character, 
one toward which a variant arises only with great difficulty and 
breeds true only in ver} 7 exceptional circumstances existing over a 
long period, such as the lactose relation. Lactose, therefore, is a 
suitable sugar in the case of typhoid, but unsuitable in the case of 

Henderson Smith.] THE TYPHOID COLON GROUP. 105 

B. coli mutdbile. Further experience will show for the different 
groups of organisms what are the carbohydrates on which reliance i.s 
to be placed as distinctive media. 

To some extent this knowledge has been already acquired. It is 
usual to make the carboh} r drate tests in fluid media with an incuba- 
tion of several days, say, from 3 to 7 days. A variant which does 
not arise in that time is probably not a very common variant, and so 
in practice our tests indicate approximately the lines along which 
further knowledge will be found to develop. The discrepancies 
which different observers occasionally record in the reactions of or- 
ganisms (e. g., the typhoid relation to dulcite and the different be- 
havior on solid and fluid media) find their explanation in this occur- 
rence of variations. 

It is not claimed by the supporters of the carbohydrate reactions 
that they are capable of giving a complete and systematic classifica- 
tion even of the intestinal bacteria according to their biological rela- 
tionships. We have at present no means of doing this with certainty. 
It must be remembered that most bacteria are extremely variable in 
other characters as well as in their sugar reactions. In pigment pro- 
duction, toxin production, gelatin liquefaction, and in practically all 
cultural reactions, variability is very frequent. Variations of viru- 
lence are amongst the oldest and commonest observations of bac- 
teriology. Even agglutinability is not a constant character, as the 
frequent occurrence of strains nonagglutinating at the time of isola- 
tion from the body is sufficient to prove. In many of these instances 
the variation consists simply of the gain or loss of a definite prop- 
erty found only with the particular species, and not in the acquire- 
ment of a character possessed by another and different species, and in 
this respect such changes may appear to differ fundamentally from 
the carbohydrate changes. (This may be not a very real distinction, 
since the carbohydrate reactions are none of them specific under 
natural conditions in the way in which, say, the toxin production of 
diphtheria is specific, but each is common to many species.) 

Such instances show that variability is one of the characteristic 
properties of bacterial protoplasm, and that systematic classification 
is likely to prove exceedingly complex. The carbohydrates do in 
large measure supply a simple method of practical differentiation of 
proved value, and it is the only method at present available which 
is sufficiently elastic to cover a large number of different organisms. 
That it does in some instances group together organisms with close 
pathological relationship is undeniable,' and there would seem to be 
no reason to doubt that as a general rule closely allied strains will 
produce similar ferments. 

It has been suggested by Reiner Midler that variabilitj^ in certain 
directions may be actually specific for certain organisms, and ho 


instances the case of typhoid, of which all strains give the isodulcite 
variation. This may be a usual or practically constant character 
of typhoid, but, as he himself recognizes, it belongs to other organ- 
isms also, and there is no known variation which is quite specific in 
the sense that it is given by every member of a species, and by no 
others. A tendency to variation in one particular direction may, 
indeed, be on occasion a useful aid in differentiating closely similar 
bacteria. R. Miiller found that paratyphoid B. produces papilla? 
on raffinose, while B. Aertryck does not. It is usual, on the conti- 
nent of Europe, to consider these organisms as strictly identical. 
Boycott, Bainbridge, and others in England hold that they are dis- 
tinct — separable by means of agglutinin-absorption tests — and it is 
an interesting confirmation of this view that Penfold, using the 
raffinose test, was able to separate a considerable number of strains 
into two groups, which practically coincided with the groups dis- 
tinguished by Bainbridge in using the absorption method. 

In the variations we have been discussing the new strain differs 
from its parent in a single character ; alteration in one character does 
not necessarily involve alteration in another. Two or more such 
variations may be superadded, but several characters do not vary 
simultaneously. Since the fermentation of the different carbo- 
hydrates is presumably due to the action of different ferments, and 
since we have no reason to suppose that power on the part of an 
organism to produce any one ferment entails either the capacity or 
incapacity to produce any other ferment, there does not appear to 
be at present any ground for anticipating that such concomitant 
variations will often be found to occur. Penfold's experiments on 
gas production, however, show that loss of a single ferment may 
affect several reactions. 3 By growing various organisms on chlora- 
cetic acid agar and selecting colonies from the plates, Penfold suc- 
ceeded, in a number of instances, in suppressing the formation of 
gas from sugars, although power to produce acid remained un- 
impaired. By this means he has bred strains of B. enteritidis Gaert- 
ner, B. paratyphosas B. B. Griinthal, and B. coli Escherlch (B. 
acidi lactici and some others remain refractory), which no longer 
produce gas from glucose. With the loss of this power went the 
loss of the gas production from various other carbohydrates. 

The extent of this loss differs a little in the case of different organ- 
isms, but, speaking generally, it was found that if an organism failed 
to produce gas from a hexose or pentose which it was able to attack, 
then it also failed to produce gas from other fermentable hexoses or 
pentoses, but might continue to produce gas from such alcohols as 
it was able to attack. The obvious interpretation of this phe- 
nomenon is that similar sugars yield as the result of fermentation 

Henderson Smith.] THE TYPHOID COLON GROUP. 107 

similar products, which are attackable by a single ferment, but that 
alcohols yield different products requiring other ferments for their 
further decomposition. This work- of Penfold has another interest, 
in that the altered strains are apparently also the strains which show 
exceptional powers of resistance to the monochloracetic acid, but the 
possible significance of this observation can not yet be fully 


It is usual to divide the bacilli of the colon -typhoid group into two 
main subdivisions according as they do or do not ferment lactose. 
This practice has the sanction of a very large experience, but it 
must be remembered that the nonlactose fermenters include one 
group of organisms (that of the B. Coli mutabile) . which are really 
more closely allied to the lactose fermenters. These organisms, 
which are more common than Massini's experience led him to believe, 
have a pronounced tendency to produce fermenting variants, and in 
fluid media most of them eventually ferment lactose, though they do 
so only late, rarely before the sixth day of growth. If the existence 
of this group is kept in mind, little practical inconvenience is caused, 
and the classification by Pactose has the advantage of bringing together 
the more definitely pathogenic organisms of the intestine hitherto 
recognized, and is not invalidated by the facts of variation, so far 
as they are yet known. None of the organisms of this division, to 
which most importance is attached in human pathology, sIioavs any 
marked tendency to produce lactose-fermenting strains, and in lab- 
oratory experience it is only by very long training that the occurrence 
of fermenting variants can be demonstrated. Further, various 
workers who have had large experience in this field have the impres- 
sion that nonlactose fermenters are in some way associated with 
abnormal conditions of the gut. The} 7 occur of course in the normal 
intestine, but in diarrheal or local inflammatory conditions they 
appear to increase in numbers relatively to the lactose fermenters. 
One may recall, in this connection, the enormous predominance of 
typhoid and dysentery bacilli which is frequently met with in the 
stools of carriers or patients suffering from these diseases. 

When the group of late fermenters and the gelatin liquefiers have 
been separated out there remains a large number of nonlactose 
bacilli, and among these one can distinguish, by cultural methods 
alone, three main groups, about which something requires to be 
said. These three groups are the typhoid, paratyphoid Gaertner 
or enteritis, and the dysentry group, and around these may be 
collected a large number of organisms, which more or less resemble 
them. There remain still a number of bacilli, which may be simi- 


larly brought together into groupings of allied members. It is quite 
probable that some of them have definite pathological importance, 
but this has not yet been clearly established for any of them. These 
have been very carefully studied by H. de R. Morgan, who over a 
series of years examined the intestinal bacilli which neither ferment 
lactose nor liquefy gelatin. His investigations were concerned chiefly 
with summer diarrhea, cholera infantum (where he found a remark- 
able association of this disease with one particular organism rarely 
occurring elsewhere, and now widely known as Morgan's No. 1), but 
they included also the intestinal flora of children, adults, and animals, 
both in the normal state and in other abnormal conditions, accom- 
panied by diarrhea or enteritis. The detailed account of these organ- 
isms is to be found in his papers, and a considerable mass of con- 
firmatory and additional information has been accumulated by other 
workers in cognate and more specialized fields of research. 

The typhoid group, — The typhoid group requires only a brief 
reference. The characters of the typhoid bacillus are well known, 
and I need only recall here that it produces acid without gas from 
glucose, mannite, and sorbite, turns milk acid without clotting it, 
and does not ferment dulcite, saccharose, nor, of course, lactose, and 
does not produce indol nor liquefy gelatin. These characters are con- 
stant for all naturally occurring strains of typhoid, with the possible 
exception of dulcite, already discussed. The B. typhosus is, in fact, 
a remarkably well-defined and stable organism. Very many strains 
have been examined in a series of carbohydrates much larger than 
the above without the detection of differences. An exception may be 
found in glycerin, since both fermenting and nonfermenting strains 
have been described, and it is probable that glycerin resembles dul- 
cite or isodulcite in being a substance to which variants are readily 
produced. But it seems beyond doubt that unless artificial means 
are taken to alter it, the typhoid bacillus is very constant in its cul- 
tural characters. All these strains, moreover, agree in their serolog- 
ical characters, and there is rarely any difficulty in identifying B. 
typhosus when it is met. Further, it is an organism to which close 
allies, as judged by the cultural reactions, do not occur naturally. 
(A somewhat similar bacillus has been found by Ledingham to occur 
frequently in flies, but it produces indol, produces alkali in milk, and 
does not ferment sorbite.) 

Nonmotile strains have been described, and strains inagglutinable 
on first isolation are comparatively frequent. If we accept, as most 
would, motility and agglutinability as definite characters of the B. 
typhosus, such strains must be accepted as subvariants, and they illus- 
trate the necessity of employing more than one criterion in identify- 
ing any organism. No one would refuse to accept as typhoid an 
organism which, otherwise typical, is at first inagglutinable, but sub- 

Henderson Smith.] THE TYPHOID COLON GROUP. 109 

sequently conforms to type after a short period of laboratory culture. 
But the duration of inagglutinability in actually observed cases is 
very variable and may extend to several subcultures. Moreover, other 
organisms, notably Gaertner's bacillus and paratyphosus B., are oc- 
casionally no less strongly agglutinated by typhoid sera than a true 
B. typhosus. Neither the presence nor the absence of the agglutina- 
tion character is in itself finally conclusive, and we must recognize 
that agglutinability is also a variable characteristic. In the case of 
typhoid, the stability of the cultural reactions and the nonoccurrence 
of organisms which closely resemble it make these reactions of especial 
value in the differentiation. 

The enteritis or Gaertner-paratyphoid group. — The second group 
is the enteritis or Gaertner-paratyphoid group, of which culturally 
the type member is the B. Gaertner. Its chief cultural characters 
which are the same as those of paratyphosus B. and B. suipestifer, 
are the following: It produces acid with gas from glucose, mannite, 
dulcite, and sorbite, does not ferment cane sugar nor lactose, does 
not produce indol nor liquefy gelatin, and litmus milk is at first made 
acid, but from about the third day on the milk turns alkaline and 
by the seventh day becomes strongly alkaline, without at any time 
clot formation or digestion. Certain other reactions will be referred 
to immediately. This group has been the subject of much confusion 
and is still the cause of a good deal of controversy. To some extent 
this is a relic of the preagglutination days, but to a still greater degree 
it is due to a loose application of the term " paratyphoid " to imper- 
fectly examined organisms. 

The cultural characters which we have detailed mark off a definite 
group of bacilli within which further distinction can be made by 
other methods, as will presently be described. But there occur in the 
normal intestine several organisms which are culturally very much 
like the type organisms of the enteritis group, but are to be definitely 
distinguished from them. Of these there are at least two main sub- 
groups, one of which ferments cane sugar and one which does not fer- 
ment dulcite. Both are comparatively common, and neither has any 
claim to the name of parat3 7 phoid. Bainbridge and O'Brien exam- 
ined a number of strains of the saccharose fermenters, which had 
been isolated by Ledingham, and while they found minor varia- 
tions in the cultural reactions they obtained no significant agglu- 
tination of any of them with Gaertner, paratyphoid B., or other sera 
made from organisms of the enteritis group. In this their expe- 
rience agrees with that of Savage and of Morgan, who also found 
the same to be true of the dulcite non fermenters. The members of 
both these subgroups are apparently quite distinct from the genuine 
enteritis organisms. Unfortunately, however, many workers, espe- 
cially on the Continent, adopt even at the present time criteria 


which do not exclude these bacteria, and by omitting dulcite, some- 
times even saccharose, from their tests they extend the name of para- 
typhoid to organisms which certainly should not receive it. This 
has led to confusion in at least two directions. On the one hand the 
epidemiology of paratyphoid fever is obscured by their inclusion in 
this group, and, on the other, the agglutination test is discredited, 
because so many so-called paratyphoid strains fail to give it. 

The organisms of these two subgroups, the cane-sugar fermenters 
and dulcite nonfermenters, are not known to have any pathogenic 
significance for man, but the pathogenic B. paratyphosus A. bears 
a close resemblance culturally to the type organisms. Paratyphoid A. 
differs from the latter only in not producing enough alkali in litmus 
milk to overcome again the initial acidity it causes. The milk turns 
acid and remains so permanently without formation of clot or true 
digestion. This organism can be readily identified by agglutination 
as well as by the milk reaction. It is not common in Europe, but 
in India it is frequently met with, and is a common cause there of 
so-called paratyphoid fever. It is not yet known whether sub- 
varieties of this organism might be distinguished by means of agglu- 
tination or other methods, but it may be noted that Morgan has 
isolated an organism identical in all respects with paratyphoid A., 
except that it was not agglutinated by a strong paratyphoid A. serum. 

There is still one other group of organisms which can be distin- 
guished from the true type organisms by cultural tests, if we extend 
them a little further. The type bacilli ferment galactose, arabinose, 
and maltose, but produce no apparent change in salicin, raffinose, or 
inulin. In the intestine of healthy animals occurs an organism which, 
resembling the type in other cultural respects, differs from it in fer- 
menting salicin. It is fairly frequent; e. g., Savage found it eight 
times in the examination of 31 animals, and its differentiation is con- 
firmed by the absence of pathogenicity and of agglutination with 
standard sera. 

When the field has been narrowed by the exclusion of these three 
subgroups, there remains the mass of organisms, which are cul- 
turally indistinguishable from the types. As was first shown by 
Durham and de Nobel e, these are separable into two very definite 
subgroups by agglutination reactions. First comes B. Gaertner, an 
organism sharply and readily differentiated by means of agglutina- 
tion, since it is not affected to any significant extent by^sera of other 
members of the group. The fact that it may be agglutinated by some 
typhoid sera, and that, conversely, typhoid bacilli may be agglu- 
tinated by Gaertner sera, causes no difficulty in identification, be- 
cause of the other characteristics of these organisms. B. Gaertner 
is the organism responsible for many attacks of food-poisoning, and 

Henderson Smith.] THE TYPHOID COLON GROUP. Ill 

it is contained in many rat viruses including B. danysz. It is be- 
lieved to have caused, and is certainly associated with, spontaneous 
outbreaks of disease in mice, guinea pigs (Bainbridge and O'Brien, 

MacConkey), and rats (Boycott), and there is some evidence that 
it is a normal inhabitant of rats and mice, or, at all events, is apt to 
develop in these animals when they suffer from depressing or toxic 
influences. What are the conditions which bring about the sudden 
epizootic virulence of the organism are unknown, but it is of in- 
terest to note that, in a similar epizootic in guinea pigs, associated 
with B. suipestifer, Petrie and O'Brien found reason to believe in 
the occurrence of a filter-passing virus. In a rat epizootic, Boycott 
isolated an organism identical with B. Gaertner in all respects, cul- 
tural, and serological (including absorption tests), which possessed 
the property of changing the haemoglobin in infected animals into 
methaemoglobin, so that their blood was chocolate or brown in color 
during life. 

The second subgroup, into which serum reactions divide the cul- 
turally typical organisms, in its turn comprises two members, the 
B. paratyphosus B. and the B. suipestifer (with the latter of which 
authorities are agreed that B. Aertryck is identical). Both organ- 
isms are agglutinated by the same sera, and to approximately equal 
degree in most cases. Manv authorities maintain that there is no 
real ground for drawing any distinction between them. Most of 
the English workers, however, and some German writers believe 
that they are separable from one another by absorption tests care- 
fully carried out, and that they are definitely distinct organisms. 
Bainbridge and O'Brien, the most recent English investigators to 
make an extended study of the subject, examined by this test a large 
number of strains from various sources, and they found that they 
fell into two groups Avhich corresponded, on the one hand, to the 
B. paratyphosus B. associated w 7 ith paratyphoid infection in man, 
and on the other to B suipestifer, associated with food poisoning. 
Their results are so consistent and clear that it is difficult to believe 
the distinction to be unreal. It has further received support from 
Penfold's application to their strains of the raffinose-papilla test 
already described, and also from complement-deviation experiments 
of H. K. Dean. 

The culturally typical organisms of the enteritis group then are 
divisible into three subgroups. B. Gaertner, paratyphosus B., and B. 
suipestifer (or Aertryck) , and into one or other of these groups fall 
all or nearly all the organisms associated with food-poisoning out- 
breaks recorded in many places since Gaertner's original description, 
as well as many of the organisms associated with animal epizootics. 
It may be noted here that the B. typhi murium is apparently not a 


separate species, but, of the organisms passing under that name, 
some are B. Gaertner and some are B. suipestifer. 

It is outside the scope of this paper to discuss the epidemiology 
of the diseases caused by these organisms, but it may be permissible 
to draw attention to the importance of always distinguishing them 
clearly. As a single illustration, it is sufficient to mention the sug- 
gestion, which their results led Bainbridge and O'Brien to put for- 
ward, that B. suipestifer and B. paratyphosus B. have a different 
distribution in nature, the former occurring in the intestine of pigs 
and other animals, the latter in the human alimentary tract. 

The dysentery group. — Some authorities, such as Lentz, maintain 
that the dysentery organisms do not really belong to the typhoid- 
colon group. Practically, hoAvever, they must be included, since they 
have to be distinguished from other intestinal bacteria which they 
closely resemble. In some respects they are the least satisfactory of 
the groups with which we have to deal, as in them we meet with a 
marked difference in grouping according as we take the cultural or 
the agglutination characters for our differentiating tests. 

One of the varieties may be dismissed quite briefly, viz, the origi- 
nal B. dysenteries of Shiga. This organism, which is nonmotile, fer- 
ments glucose without production of gas, and, after preliminary acidi- 
fication, turns milk alkaline on or soon after the third day. It does 
not ferment mannite, dulcite, cane sugar, lactose, nor sorbite, and does 
not produce indol. A somewhat similar organism has been described 
by Morgan, but it is motile and produces indol, and the agglutination 
reactions of the Shiga bacillus are characteristic. 

It is when we come to the mannite-fermenting types of dysentery 
bacilli that difficulties arise. Some doubt has been expressed as to 
their claim to be considered genuine dysentery bacilli at all, owing to 
an alleged milder clinical course of the disease with which they are 
associated, but they frequently produce extremely severe or fatal dys- 
entery, and a doubt of this kind is unjustified. An individual posi- 
tion is taken amongst them by the bacillus of Strong. This organism 
is unlike the rest in fermenting dulcite and cane sugar and in pro- 
ducing clot in milk, and its agglutination reactions also separate it 
from the others. As it has apparently been only once found in asso- 
ciation with dysentery, it is of subordinate importance, but we may 
notice that organisms not very dissimilar culturally and agglutinated 
by Strong serum have been found by Morgan to occur in the stools 
of typhoid convalescents. 

The representative organism of the mannite-fermenting type is 
Flexner's B. dysenteric and it is the best known member of a group 
which possesses the following general characters: They are nonmotile, 
ferment glucose and mannite without production of gas, turn milk 

Henderson Smith] THE TYPHOID COLON GROUP. 113 

alkaline after preliminary acidification, produce indol, and do not 
ferment lactose, dulcite, or cane sugar, and do not liquefy gelatin. 
These group characters are possessed by most of the mannite-fer- 
nienting dysentery organisms, though variations occur in the readi- 
ness with which they produce alkali in milk and form indol. Whether 
all intestinal organisms with these characters are potential producers 
of dysentery can not be definitely stated as yet. It seems improbable, 
since they occur not infrequently in individuals with no history of 
dysentery, but sufficient evidence on the point is lacking. It is ap- 
parently questionable whether agglutinability by Shiga, Strong, Flex- 
ner, or even by Y., serum is a necessary property of all the patho- 
genic members of the group. 

Flexner's organism ferments maltose and dextrin, and does not 
ferment sorbite, but other members of the subgroup show differences 
in one or more of these characters. This has recently been clearly 
shown by Morgan, who examined the behavior toward 18 carbohy- 
drates of over 50 strains, and it has also been brought out by Teb- 
butt in his study of institutional dysentery in England, as well as 
by others. The best known of these, the Y. bacillus of Hiss and 
Russell, does not ferment maltose in its original state, and this 
sugar has therefore been used as a basis of subclassification. We 
know, however, from Hiss's own work that the Y. organism readily 
acquires the power of fermenting maltose, and there are other 
grounds for doubting the stability of the character. Bacillus Y. 
resembles B. Flexner much more closely than do some other unde- 
niable dysentery strains, e. g., some of the El Tor organisms of 
Ruffer and Willmore; and a primary subdivision on a maltose basis, 
even if the character were less variable than we know it to be, would 
separate Y. and Flexner, while bringing together other organisms 
much less closely alike. It would appear to be more satisfactory to 
adopt a subdivision according to the more stable sorbite character, 
as suggested by Tebbutt, and to redivide the subgroups, so formed, 
into those which do and those which do not ferment dextrin. This 
gives us four groups, each of which contains some dysentery organ- 
isms. It brings the Y. bacillus into the same subgroup with the true 
Flexner, from which it can, if desired, be distinguished by the maltose 

By no system of classification, however, can we bring the cultural 
and serological reactions into harmony. It appears that motile 
bacilli with claims, on cultural grounds, to admission to the group, 
are definitely not agglutinated by dysentery sera, but, otherwise, the 
results are quite discordant, All observers are agreed that absorption 
methods are unsatisfactory for these organisms, and in every sub- 
group there occur ome strains which are agglutinable by Flexner 
66692— vol 2, tt 1—13 8 


serum and some which are not. We must recognize the fact that 
the biochemical and serum reactions are not at one in this group. 
Of course there is really no a priori ground for expecting them to 
agree, since variation in one character is not necessarily accomplished 
by variation in another. Between the two conflicting methods of 
classification, we have no conclusive reason for preferring the one 
to the Qther, and we must wait for further experience on the subject. 
The impression one gains is that the dysentery organisms, as a group, 
are in a very unstable condition, and have not acquired fixed char- 
acters such as we find in other bacilli of the typhoid-colon class. A 
thorough examination of representative members, from the mutation 
or variation point of view, is much to be desired. 

The details which have been given in the preceding pages of this 
section enable us accurately and easily to subdivide such of the 
organisms of the typhoid-colon group as do not ferment lactose and 
do not liquefy gelatin into a number of distinct subgroups. The 
members of each subgroup resemble each other more or less closely, 
but they admit of a further subdivision by methods which are in most 
cases readily practicable. The resulting classification is summarized 
briefly in the following table : 


I. Late lactose fermenters. 

II. Certain groups of no known pathogenic importance. 
III. Typhoid group. 
IV. Paratyphoid-enteritis group : 

1. Atypical members : 

(a) Saccharose fermenters. 
(6) Dulcite nonfermenters. 

(c) B. para typhosus A. 

(d) Salicin fermenters. 

2. Typical members : 

(a) B. enteriditis Gaertner distinguished from (b) and (c) by 


(b) B. paratyphosus B., distinguished from (c) by absorption. 

(c) B. snipestifer. 
V. Dysentery group: 

1. Mannite nonfermenting. B. dysenteriae Shiga. 

2. Mannite fermenting: 

(a) B. dysenteriae Strong. 

(b) Sorbite fermenters. 

(i) Dextrin' nonfermenting. 
(ii) Dextrin fermenting. 

(c) Sorbite nonfermenters. 

(i) Dextrin nonfermenting. 
(ii) Dextrin fermenting. 

(a) Maltose fermenting (B. dysenteriae Flexner). 

(b) Maltose nonfermenting (B. dysenteriae Y). 

HeDdersoD Smith.] THE TYPHOID COLON <;ROUP. 115 


In conclusion, there are one or two general considerations which 
1 wish to bring forward. The amount of work which is done in con- 
nection with the typhoid-colon group every year, and in all parts of 
the world, is simply enormous. Even if we omit the routine examina- 
tions of such material as water, the work devoted to the investiga- 
tion of faeces alone in connection, with carriers, food poisonings, en- 
teritis cases, genuine or suspected, and so on, is immense. This repre- 
sents a large expenditure of energy, and, unfortunately, much of it 
does less than it might to advance our knowledge of bacteriology and 
the epidemiology of intestinal disease. There is a waste of energy 
in two directions. On the one hand, much time and labor are in 
many cases expended on the elaboration of points which contribute 
little or nothing to establishing the identity of the organism studied, 
and, on the other, much of what is considered by many to be essential 
to its complete description is too often omitted. 

The early bacteriologists, for want of other diagnostic tests, were 
compelled to lay stress on the appearance of colonies on the ordinary 
media, their vine-leaf shape, prominence, moistness, translucency, 
and so on. Such points as these are of almost no value as differential 
tests. Even a blue colony on Conradi-Drigalski is of only elementary 
differential value, and the appearance of such colonies, their exact 
shade of blueness, etc., does not take the distinction beyond the 
primary division into lactose fermenters and nonlactose fermenters. 
But we still quite frequently find these details set out with laborious 
minuteness as if they contributed essential information in the dis- 
tinction of the group members from one another. Lengthy descrip- 
tions of this kind do not repay the trouble they demand, and will no 
doubt gradually disappear in time; but we are threatened with an- 
other cause of waste of energy in the multiplication of tests. The 
introduction of new tests is most desirable, for by them we may hope 
to deepen our knowledge, but when a test has received an extensive 
trial and has contributed nothing fresh to our knowledge, it should 
be dropped again. There are certain complicated media, for example, 
in frequent use for the growth of typhoid bacilli which might very 
well lapse into disuse. 

On the other hand, I would urge a more general recognition of the 
value of the carbohydrate media. These tests supply most valuable 
help in the differentiation of the typhoidlike bacteria from one another. 
This is true of all the subgroups, but they are especially important in 
the case of the Gaertner-paratyphoid group, where we meet so many 
organisms closely resembling the genuine pathogenic bacilli. Yet 
we find bacteriologists, even of great and deserved repute, classifying 
organisms whose dulcite or saccharose reactions have not been 


studied as identical in fermentation activity with paratyphoid B. 
Possibly they look on these points as of minor importance, but the 
want of information of this kind greatly reduces the value to others 
of the work done ; and handicaps them in subsequent investigations 
on similar lines. 

This is an excellent illustration of what really constitutes at present 
a great part of the difficulty which these organisms present, viz, the 
lack of uniformity in the methods by which they are studied. Bac- 
teriologists in different countries, and in different parts of the same 
country, rely on different criteria in establishing a diagnosis, and, as 
a consequence, neglect the tests in which they happen to place less 

To some extent this is inevitable, but it has the result of making 
the information collected by the followers of one set of criteria in- 
adequate and therefore largely useless to those who adopt another 
set. Now, taken altogether, the number of tests employed by the 
leading bacteriologists who have devoted much time to the study of 
these intestinal bacilli is not very large, and it should be possible for 
all workers to adopt as a basis a uniform standard of minimum re- 
quirements. This standard would not be exhaustive in the sense of 
including all known tests, and individual workers would naturally 
add other tests, either old or new, to which they attached importance. 
It need have nothing dogmatic about it, and would not commit those 
who adopted it to a belief in 'the validity of all the tests it included, 
and it would be subject to revision from time to time. But it would 
be comprehensive enough to cover all the most important tests on 
which bacteriologists of different schools are accustomed to rely. It 
would, therefore, insure that work done in one part of the world by 
one school would be available to other schools elsewhere, and we 
should avoid the very real present difficulty, that the work of any 
one school is of full value only to that school and to no other. Some- 
thing of this kind seems very much to be desired. Naturally, it 
could be drawn up only by an association, at which the different 
methods of examination were adequately represented. If this section 
of the International Congress of Hygiene and Demography were to 
appoint a representative committee to draft recommendations of the 
nature indicated it would take a step which it is well qualified to 
take and one which would be of great value to all bacteriologists. 


It is scarcely possible to summarize this paper briefly, but its 
scope may be indicated by the following: 

Mutation or variation, as it occurs in members of the typhoid- 
colon group, is discussed in some detail, and it is pointed out that, 

Henderson Smith.] 


while many members of the group are capable of such alteration 
toward one or more carbohydrates, this does not occur haphazard 
but in certain directions which are definite for each organism. An 
organism produces with greater readiness variants toward some 
carbohydrates than to others, and the more disposed an organism is 
to produce a particular variant, the more readily does it take the 
new character permanently. Variability is one of the characteristics 
of bacteria, and affects most of their known properties, and the fact 
that variation occurs toward carbohydrates does not invalidate their 
use as aids to differentiation. The carbohydrate media are the most 
elastic, most practical, and most satisfactory means at present avail- 
able of distinguishing the members of this group. 

The primary division being made into those which do and those 
which do not ferment lactose, the nonlactose fermenters, which in- 
clude the important pathogenic members, are considered in detail. 
The three prominent groups of typhoid, paratyphoid, Gaertner, and 
dysentery, are taken separately, and their characters, and those of the 
organisms most closely resembling them, are set out. Finally, a plea 
is put forward for greater uniformity, and, if possible, some stand- 
ardization of the methods employed in their study. 


Bainbridge, Proc. Roy. Soc. Medicine, Epidemiology Sect., February, 1911. 

Bainbridge and O'Brien, Journal of Hygiene, 1911, XII, p. 24. 

Boycott. Journ. of Hygiene, 1911, XI, p. 443. 

Burk, Arch, fur Hyg., 1908, G5, p. 235. 

Hiss, Journ. Med. Research, 1904, XIII, p. 36. 

Jacobsen, Centralb. f. Bakt, 1910, Orig. 56, p. 206. 

Ledingham, Journ. of Hyg., 1911, XI, p. 333. 

Massini, Arch. f. Hyg., 1907, 61, p. 250. • 

Morgan, D. de R., Bacteriology of summer diarrhea, Brit. Med. Journ., 1906, 
I, p. 90S; ibid., 1907, II, p. 16; the mannite-fermenting group of B. dysenterw, 
Journ. of Hyg., 1911, XI, p. 1. 

Morgan and Ledingham, Bacteriology of summer diarrhea, Proc. Roy. Soc. 
Med. (Epidemiol. Sect), 1909, II, p. 133. 

Miiller, Reiner, 1908, Centralbl. f. Bakt. 42, p. 57; 1909, Munch, med. Woch., 

1909, p. 885 ; 1911, Centralbl. f. Bakt., 58, p. 97. 

Penfold, W. J., 1910: Bacterial variation, Journ. Path, and Bact, XIV, p. 406, 
1910; Variations of fermentation properties of B. typhosus, Brit. Med. Journ., 

1910, II, p. 1672; 1911, Variability in gas-forming power of intestinal bacteria, 
Proc. Roy. Soc. Med. (Path. Sect.) and Journ. of Hyg., XI, p. 487; 1911, Studies 
in bacterial variation, Journ. of Hyg., XI, p. 30; 1912. Specificity of bacterial 
mutation, Journ. of Hyg., XII, p. 195. 

Petrie and O'Brien, Journ. of Hyg., 1910, X, p. 2S7. 
Ruffer and Willmore, Brit. Med. Journ., 1909, II, p. 862. 
Savage, Journ. of Hyg., 1912, XII. p. 1. 


Tebbntt, ibid., 1912, XII, p. 218. 

Twort, Proc. Boy. Soc, 1907, Series B, vol. 79, p. 329. 

\At the Berlin meeting of this Congress, in 1907, certain institutes were re- 
quested to undertake an inquiry into the differentiation of the " typhoidlike " 
bacteria, and to present a report upon these organisms at the Washington meet- 
ing this year. This paper constitutes the report of the Lister Institute of Pre- 
ventive Medicine, London. 

2 The converse is not necessarily true, however, since all strains of typhoid 
produce papillae on isodulcite, but lose this character readily, and no strain has 
yet been isolated which is already in the nonpapilla-forming state. 

3 With this may be compared the nongas-producing B. Aertryck recorded by 


M. le Dr. Sacquepee, Professeur au Val-de-Grace, Paris, France. 


Sous la designation commune de bacilles paratyphiques, on s'est 
accoutume et on continue a comprendre des especes microbiennes 
certainement differentes. 

A tous points de vue, le bacille paratyphique A et le bacille 
paratyphique B doivent etre separes Fun de l'autre. 

Nous nous occuperons exclusivement du bacille paratyphique B et 
des especes, ou tres voisines, ou identiques. 

A. l'ensemble de ces especes, nous avons deja donne le nom de 
Salmonelloses, du nom de Salmon, qui a decrit, sous le nom de bacille 
du hog cholera, le premier representant du groupe. 

1°. Les carjfcteres culturaux et morphologiques, communs a tous 
les Salmonelloses, sont connus, et il nous parait inutile a y insister. 

2°. Les reactions biologiques (proprietes des serums) divisent le 
groupe des Salmonelloses en deux sous-groups: 

a. Sousr-groupe I. Comprenant comme type le plus important le 
bacille d'empoisonnements alimentaires (ou bacille carne) de Gartner. 

b. Sous-groupe II. Numeriquemerit beaucoup plus repandu, com- 
prenant entre autres: Le bacille carne du type aertrycke; le bacille 
paratyphique B des infections par typhoides humaines; le bacille 
de la'psittacose; le virus Loeffler; quelques echantillons de hog cholera 
(echantillons Salmon). 

D'une maniere generale, le serum specifique pour le sous groupe 
I. presente une agglutinine et une sensibilisatrice specifiques pour 
tous les representants du sous groupe I ; ces memes serums n'ont pas 
d'action bien nette sur le bacille du sous groupe II. 

Inversement, les serums specifiques pour l'une quelconque des 
especes du sous groupe II presentent une agglutinine et une sensi- 


bilisatrice sp6cifiqnes pour toufi les representants du sous groupe II. 
Le degre d'activite des serums peut etre un peu variable suivant les 
especes, sans que cette inegalite d'action permette de les separer nette- 
ment les unes des autres. 

L'epreuve de la saturation ne les separe pas da vantage. 

Les serums du sous groupe II ne manifestent aucune action 
specifique a l'egard des bacilles du sous groupe I. 

3°. Les caracteres culturaux et morphologiques des salmonelloses 
ne sont pas a eux seuls suffisarits pour la delimitation du groupe; 
tous, sans exception, y comprit le cameleonage du lait et du petit lait 
tournesoles, peuvent appartenir a des varietes de paracolibacilles, ne 
hog cholera avec les Salmonelloses. 

Appartiennent exclusivement a ce groupe, les microbes qui pre- 
sentent, outre les caracteres morphologique et culturaux indispensa- 
bles, la propriete d'etre agglutinos a dose convenable ou de provoquer 
la deviation du complement en presence de l'un ou l'autre des deux 
serums specifiques signales plus haut. 

4°. On a discute et on discute encore sur la parente des bacilles du 
hog cholera avec les Salmonelloses. 

En fait, il parai etabli que les bacilles dits du hog cholera ne con- 
stituent pas l'agent specifique de cette maladie ; ils ne representent que 
des infections secondaires. Comme tels, on congoit qu'ils puissent ne 
pas constituer une espece, mais bien un groupement heterogene de 
microbes varies. 

Seule appartient a notre cadre la variete decrite originellement 
par Salmon. 



L'expansion des Salmonelloses est considerable. 
1°. Chez l'homme, a l'etat pathologique, dans deux series de circon- 
stances cliniquement differentes. 

(a) Au cours des infections paratyphoides, ces microbes peuvent 
etre deceles dans le sang, dans la plupart des organes, dans les excreta 
(selles^ i^rines). 

Ils peuvent persister dans les selles pendant quelque temps apres 
la guerison. 

(b) Au cours des empoisonnements alimentaires ; les Salmonelloses 
existent, generalement en grande quantite, dans le contenu intestinal, 
dans le contenu gastrique; elles ne passent dans le sang que chez les 
sujets atteints de formes extremement graves. 

2. Chez les animaux malades. — (a) Chez les animaux boucherie, 
susceptibles de presenter pendant la vie des lesions extremement 
variees. Diarrhee infectieuse, phlebite ombilicale, pyohemie, chez 
le veau; diarrhee, metrite, chez la vache; abces, chez le pore; abces, 
enterite, chez le cheval. 


(b) Au cours d 'epizootic chez les rongeurs, rats, seuris, cobayes, 
etc. * * * 

3. Dans les aliments contamines les plus divers: viande, legumes, 
poisson, cremes de patisserie, etc. 

4. Exceptionnellement, on peut rencontrer les memes microbes, en 
dehors de tout etat pathologique appreciable, soit chez l'homme, soit 
chez diverses especes animales, specialement les animaux de boucherie. 


Nous devons insister specialement sur la bacteriologie des aliments 

Les aliments animaux susceptibles de nous interesser sont : la viande 
et le lait. 

(A) Viandes. — On peut rencontrer des Salmonelloses dans deux 
circonstances differentes : 

Dans la viande provenant d'animaux infectes (viande malade). 

Dans la viande qui, provenant d'animaux sains, a ete contaminee 
apres abattage (viandes contaminees). 

1°. Viandes malades. — Comme il a ete dit ci-dessus, il est etabli 
que certaines affections des animaux de boucherie sont provoques par 
des Salmonelloses, specialement chez le veau, la vache : le boeuf, le 
pore, le cheval. 

En pareil cas, les microbes se rencontrent, non seulement dans les 
lesions locales, mais encore dans tous les organes et dans la chair 
musculaire. II s'agit en realite d'une septicemic Cette derniere se 
manifeste parfois par une pullulation des microbes a l'interieur meme 
des vaisseaux. 

La viande et les visceres de ces animaux : inferes par l'homme, pro- 
voquant chez lui des empoisonnements alimentaires. 

II convient en outre de noter : 

(a) Que, sous certaines observations, l'examen apres abattage n'a 
permie de deceler aucune lesion appreciable, bien que l'animal fut 
certainement infecte, la viande renfermant des Salmonelloses et ay ant 
provoque des accidents toxiques. 

Le fait n'a rien de surprenant pour des microbes a cet ordre, 
qui sont aptes autant que nul autre a provoquer des septicemics, 
sans lesion grossiere apparente, a l'instant des infections paraty- 
pho'i'des humaines. En pareil cas, on ne pourrait etre appele a soup- 
Qonner un etat pathologique qu'en soumettant l'animal a une observa- 
tion sanitaire pendant quelque temps avant l'abattage ; 

(b) Que la chair musculaire des animaux infectes peut ne presenter 
aucune alteration appreciable ; 

(c) Que la cuisson diminue general ement la toxicite des viandes 
infectes, sans toutefois la faire disparaitre completement. 


(d) Que certaines especes animales, specialement le mouton, sont 
tres rarement infectes par les Salmonelloses. 

II semble ressortir de certaines recherches, qui d'ailleurs attendent 
confirmation, qu'on pourrait trouver exceptionnellement des Sal- 
monelloses dans la viancle saine provenant d'animaux sains, surtout 
quand ces derniers ont ete surmenes avant l'abattage. Le fait n'a rien 
d'impossible, car il est connu qu'a la faveur de toute diminution de la 
resistance de l'organisme les microbes preexistants dans l'intestin 
peuvent emigrer dans la circulation generale. 

De semblables constatations interessent plus la biologie generale 
que l'hygiene; car il est vraisemblafle que ces quelques microbes 
epares dans les tissus peu ou pas alteres n'y rencontrent que des 
conditions defavorables a leur developpement ou meme a leur simple 
persistance. Experimentalement, les septicemics que nous avons 
provoquees dans des conditions tres analogues se sont toujours 
montrees ephemeres et benignes. 

'2°. Viandes contaminees. — Une viande, primitivement saine, peut 
se tf ouver contaminee par des mecanismes tres varies. 

La contamination est d'autant plus facile que les elements de la 
viande constituent le milieu nutritif par excellence, couramment em- 
ploye en bacteriologie. 

Les chances de contamination sont d'autant plus grandes que la 
viande est soumise a des manipulations plus nombreuses; aussi, les ali- 
ments contamines se recrutent — ils se trouvent generalement parmi 
les viandes dites travaillees: hachis, saucisses, cervelas, pates, et pro- 
duits divers de charcuterie. 

Les produits de charcuterie sont d'autant plus menaces que 1'ad- 
jonction d'ingredients varies permet d'y incorporer des viandes 
douteuses ou avancees, dans lesquelles les germes de toutes natures 
ont pu se multiplier a loisir. 

La contamination est susceptible d'etre provoque par plusieurs 

(a) L'une quelconque des personnes appelees a manipuler les ali- 
ments peut etre infectee. L'infection se traduit chez elle par une 
infection benigne, telle que l'embarras gastrique, trop benigne pour 
entraver les occupations habit uelles; ou bien il s'agit d'une infection 
plus grave, soit avant, soit apres revolution des symptomes severes. 
Dans ces diverses circonstances comme nous l'ont demontre nombre 
d'episodes epidemiologiques, le sujet infectieux peut contaminer tous 
les ailments, y compris les viandes. La contamination se fait prob- 
ablement par l'intermediaire des mains, si l'interesse ne prend pas 
quelques precautions elementaires de proprete. 

(b) Au meme titre, les ailments peuvent etre contamines par des 
porteurs de bacilles paratyphiques. La plupart de ces derniers ont 
ete atteints anterieurement d'une affection paratyhoide, parfois fruste 


et meconnue. lis peuvent demeurer contagieux pendant plusieurs 

(c) Le contact d'une viande saine avec une viande infectee, ou 
bien avec des instruments ou des ustensiles maipropres, suffit a provo- 
quer la contamination de quantites importantes d'aliments. Ce mode 
de contamination intervient tout specialement dans le commerce de 
la charcuterie, ou les melanges sont frequents et les manipulations 

Quelques auteurs ont avance qu'on trouvait assez souvent des bacilles 
paratyphiques dans des aliments parfaitement sains contamines, sans 
danger pour l'homme. La chose est possible; il n'y a rien d'invrai- 
semblable a ce qu'il existe dans les milieux exterieurs des Salmonel- 
loses inoffensives pour l'homme. Toutefois, les experiences apportees 
a l'appui de cette conception ont ete depuis plutot infirmees que con- 
firmees, et par suite on ne pent les considerer comme irrefutable^. 
D'autre part, les echantillons de microbes rencontres en pareil cas, 
tout en presentant les caracteres cultureux et morphologiques des 
Salmonelloses, n'ont generalement pas ete sounds au controle* de 
Taction specifique des serums, qui constitue un criterium indis- 
pensable. La question reste a l'etude et merite d'etre suivie. 

Pour le moment, nous ne pouvons pas considerer comme suspecte 
toute viande, travaillee ou non, infestee par des Salmonelloses bien 
caracterisees. L'experience nous a trop nettement demontre que de 
tels aliments sont d'ordinaire toxiques pour l'homme. 

(B) Lait. — Comme pour la viande, le lait peut etre infecte soit 
par suite d'une maladie de l'animal, soit par suite d'une contamina- 
tion acciden telle : 

1°. En cas de mammite, provoquee par les Salmonelloses, chez la 
vache, le lait peut etre profondement infecte. 

2°. Un lait, pur a l'origine, peut etre contamine ulterieurement : 

(a) Par l'un ou l'autre des mecanismes indiques a propos de la 

(b) Par addition d eau souillee. 

Les bacilles paratyphiques peuvent passer dans les eaux avec les 
dejections, les urines, les eaux de lavage de boucheries, d'abbatoirs, 


L'homme, tres receptif a l'egard de la plupart des Salmonelloses, 
peut etre infecte de diverses manieres. 

1°. Par contagion directe de rwalade a sujet sain. — Cette contagion 
directe est beaucoup plus frequente dans les infections paratyphoides 
que dans les empoisonnements alimentaires. 

C'est remarquable de constater que la forme clinique des atteintes 
secondaires, par contact, est generalement identique a l'atteinte primi- 


tive, contagionnante. Une infection paratyphoi'de donne naissance 
an syndrome d'infection paratyphoi'de, et non pas au syndrome d'em- 
poisonnement alimentaire; il en est de meme, mutatis mutandis, < i n 
cas de contagion secondaire des empoisonnements alimentaires. 

2°. Par contagion indirecte. — Cette contagion se fait par l'inter- 
mediaire des aliments infectes. 

(a) L'infection peut venir de l'homme lui-meme: contagion des 
aliments par le personnel appele a les manipuler; contamination des 
eaux de boisson, des eaux de lavage, etc. Les formes cliniqnes ob- 
servers en pareil cas sont tres variables; tantot infection paratyphoi'de. 
tantot empoisonnements alimentaires. 

(b) L'aliment, provenant d'nn animal malade, peut etre infecte 
d&s I'origine. De tels aliments engendrent regulierment chez l'homme 
des empoisonnements alimentaires. 


1°. Au point du vue clinique, les affections provoquees par les Sal- 
monelloses chez l'homme ou chez les animaux sont des plus disparates. 

Entre ces di verses Salmonelloses, la bacteriologie ne reconnait 
cependant actuellement aucune difference appreciable ; il en est ainsi 
particulierement du bacille paratyphique B des infections paraty- 
phoides humaines et du bacille type aertrycke des empoisonnements 

Cette diversite de reaction clinique en presence de microbes en ap- 
parence identiques est un peu troublante. 

Pour l'expliquer, Trautmann en fait appel a une conception in- 
genieuse bien connue. " L'intoxication par la viande est une forme 
aigiie, le paratyphus une forme sub-aigiie, d'une maladie infectieuse, 
une au point de vue etiologique." C'est-a-dire que l'ingestion de 
microbes en petite quantite, susceptibles des pullules peu a peu dans 
l'intestin, determinerait un malade a evolution relativement lente; 
tandis que l'affection aigue succederait a l'ingestion d'une grande 
quantite des memes microbes avec leur toxine. 

Cette conception me parait en partie exacte; toutefois, elle n'ex- 
plique pas tout. 

Diverses raisons empruntees, partie a l'observation, partie a l'ex- 
perimentation, amenent a croire qu'en realite certaines Salmonelloses 
tout douees originellement de proprietes toxiques, qui font defaut 
chez d'autres; et inversement, ces dernieres peuvent etre douees de 
proprietes infectieuses, marquees par leur tendance a la generalisa- 
tion, qui sont exceptionnelles chez les jDremieres. 

Malgre leur identite apparente, j'estime que les bacilles carnes et 
les bacilles paratyphiques doivent etre considered comme pourvus 
de fonctions biologiques un peu differentes, les premiers surtout 
toxiques, les seconds surtout infectieux. 


Ces differences biologiques sont d'ailleurs surtout accusees dans 
les types extremes, entre lesquels il existe certains intermediates. 

2°. D'autre part, parmi les Salmonelloses il existe certainement des 
especes pen virulentes pour l'homme. II semble en etre ainsi en par- 
ticulier de la plupart des virus des rongeurs. Ces derniers, en effet, 
malgre le commerce considerable dont ils sont Fob jet, ne paraissent 
avoir infecte l'homme que d'une maniere exceptioniielle. La rarete 
meme cle ces infections suffit a montrer que tout au moins des nuances 
biologiques separent ces virus des Salmonelloses habituellement pa- 
thogenes pour l'homme ; l'existence indeniable des accidents qu'ils peu- 
vent provoquer chez l'homme suffit d'autre part a demontrer que ces 
nuances biologiques ne sont pas irreductibles. 

3°. L 'experience a montre que la viande des pores atteints de 
pneumo-enterite n'est toxique pour l'homme que d'une maniere ex- 

On peut accepter a l'heure actuelle que la toxicite existe exclusive- 
ment dans le cas ou il s'est produit une infection secondaire par le 
bacille de Salmon. En toute autre circonstance, la viande peut etre 
contaminee sans danger. 

A cet egard, l'histoire du cholera du pore est identique a celle de la 
diarrhee, de la pyohemie, du veau, des abces du cheval, etc.; ces 
diverses maladies infectieuses sont en effet susceptibles d'etre pro- 
voquees par des microbes varies; la viande n'est dangereuse que si 
Tagent infectieux est pathogene pour l'homme. 

4°. La comparaison des faits suggere l'opinion que les Salmonelloses 
se sont accoutumees peu a peu a telle ou telle espece animale, a l'egard 
de laquelle elle se montre particulierement offensive dans les condi- 
tions naturelles : bacille paratyphique B chez l'homme, bacilles carnes 
chez les bovides, virus des rongeurs chez les rongers, etc. Mais ces 
fixations relatives n'ont rien d'absolu, et ces memes microbes sont 
aptes a infecter d'autres especes animales, quand les circonstances s'y 
pretent ; et l'homme, en raison de son alimentation carnee, y est parti- 
culierement expose. 


1°. A V egard des individus contagieux. — (a) II est necessaire de 
soumettre a l'isolement tout individu atteint d'une infection provoquee 
par les Salmonelloses. 

Les malades presentant la forme clinique dite infection paraty- 
phoi'de ne doivent pas etre melanges avec les malades atteints de 
fievre typhoide. 

II serait desirable que l'isolement soit maintenu jusqu'a ce que les 
bacilles nient certainement disparu des excreta. 

On prendra les merries mesures de disinfections qu'a l'egard de la 
fievre typhoide. 


(b) Certaines professions meritent une attention speciale, en raison 
de ce que leurs adherents prennent part a la manipulation des ali- 
ments; specialement le personnel des boucheries, charcuteries, des 
cuisines, des services des restaurants et hotels, etc. 

On a le droit de demander que dans les etablissements ou verts au 
public, tout ce personnel soit soumis a une surveillance medicale 
constante, tant au moment de l'embauchage que pendant la duree de 
son service. Au premier signe d'infection, tout individu suspect 
serait eloigne et soumis a un examen medical et bacteriologique, dont 
les resultats dicteraient la mesure a prendre. Une indemnite raison- 
nable serait attribue a l'interesse. 

2°. A Fegard des animaux malades. — La surveillance sanitaire de 
tout animal destine a 1'alimentation humaine est indispensable. 

(A) Elle doit etre pratiquee: 

(a) Avant l'abattage, pour reconnaitre les symptomes, diarrhee, 
etat febrile, de certaines maladies qui peuvent ne determiner aucune 
lesion anatomique appreciable. 

(b) Apres l'abattage, en vue de deceler toute lesion pathologique. 
Pour chaque animal suspect, il serait necessaire de proceder a 

l'examen bacteriologique (examen direct, culture) du tissu muscu- 
laire, du foie et de la rate. L'existence en quantite appreciable de 
bacilles appartenant certainement au groupe des Salmonelloses en- 
trainerait la saisie totale (la sterilisation par la chaleur est insuffi- 
sante), avec indemnisation du proprietaire. 

(B) L'application stricte de la surveillance sanitaire des animaux 
exige une inspection obligatoire et generalisee. 

Elle doit etre organisee dans les pays ou elle n'existe pas encore. 

Cette inspection ne peut etre assuree que par des personnes compe- 
tentes, veterinaire, ou a defaut, medecin. II est illusoire et il pourrait 
etre dangereux de confier un tel service a des personnes d'une com- 
petence douteuse. 

^inspection. — Afin de permettre le fonctionnement du service d'ins- 
pection, les abattages ne doivent avoir lieu qu'exclusivement dans des 
abattoirs publics, soumis a une surveillance permanente. Comme con- 
sequence, suppression complete des tueries particulieres. 

3°. A Vegard des industries de travail ou de debit des viandes 
{charcuteries\ etc.). — (a) En ce que concerne l'etat de sante des per- 
sonnes, il serait necessaire de les soumettre au regime prevu en 1° (b) 

(b) La proprete la plus meticuleuse sera constamment observee, 
tout en ce qui concerne les soins corporels des personnes que l'entre- 
tien des instruments, utensiles et locaux. 

(c) On interdira avec la derniere rigueur l'emploi de yiandes de 
mauvaise qualite. 


(d) La creation d'ateliers centraux de charcuterie, preconisee de 
divers cotes, pour faciliter la salubrite des operations et la surveil- 
lance sanitaire est une ceuvre logique et recommandable. 

4°. Precautions familiales. — (a) Les personnes qui utilisent les 
virus des rongeurs seront prevenues du danger eventuel de ces virus 
pour l'homme et des mesures a prendre pour eviter tout accident. 

(b) Dans tous les pays ou les empoisonnements par les Salmonel- 
loses sont quelque peu frequents, il est indique de limiter au strict 
minimum la consommation de viande a, l'etat cru. Le public doit 
etre reseigne a cet egard. 


I. Les Salmonelloses comprennent comme especes principales les 
bacilles d 'empoisonnements alimentaires (types Gartner et type 
Aertrycke), le bacille paratyphique B, les virus des ronjeurs, quelques 
echantillons de bacilles du hog cholera. 

L'action des serums specifiques separe les Salmonelloses en deux 

Appartiennent exclusivement aux Salmonelloses les microbes qui 
presentent, outre les caracteres generaux indispensables, la propriete 
d'etre agglutines ou de provoquer la deviation du complement en 
presence de Fun ou l'autre des serums specifiques pour chacun des 
deux sous-groupes. 

II. Les Salmonelloses sont tres repandues. On les rencontre entre 
autres: Chez l'homme malade, dans les infections paratyphoides et 
les empoisonnements alimentaires ; chez les animaux de boucherie, au 
cours de maladies diverses; dans certaines epizooties des rongeurs; 
dans divers aliments contamines; parfois chez l'homme ou les ani- 
maux a l'etat sain. 

III. Les aliments animaux le plus frequemment infectes sont les 
viandes et le lait. 

(A) Viandes. — L'infection peut provenir de ce que l'animal etait 
atteint d'une maladie provoquee par une Salmonellose ; ce sout les 
viandes dites malades. La maladie de l'animal peut s'accompagner 
ou non de lesions anatomiques appreeiables. Dans tous les cas, c'est 
la septicemic qui coustitue le phenomene le plus important. 

La presence eventuelle de Salmonelloses dans la viande d'ani- 
maux sains n'a rien d'impossible, mais ne parait pas constituer un 
danger sanitaire serieux. 

Une viande primitivement saine peut etre infectee apres abatage 
(viande- contaminees) . Les mecanismes de contamination sont tres 
varies: il faut citer en premiere ligne le role des personnes appelees 
a manipuler les aliments dans les cuisines, les charcuteries, etc. La 
contamination pent se prodiiire egalement par contact avec des ali- 
ments infectes. avec des instruments malpropres, etc. 


II n'est pas demon t re que des Salmonelloses bien caracterisees 
puissent exister dans les aliments sans provoquer d'accidents. 

(B) Lait. — Memes mecanismes de contamination que pour la 
viande. En plus, contamination par l'eau souillee. 

IV. L'homme pent contracter des infections a Salmonelloses, 
soit par contact direct, soit par ingestion d'aliments ou d'eaux con- 

V. Les diverses Salmonelloses, identiques les unes aux autres devant 
la bacteriologie, different probablement par certaines proprietes 

VI. La prophylaxie doit viser: 

(a) L'individu contagieux: isolement disinfection. 

(b) La surveillance sanitaire de tous les individus prenant part 
aux professions alimentaires. 

(c) La surveillance des animaux de boucherie, avant et apres 
Pabatage, avec inspection obligatoire et generalises. 

(d) La surveillance des ateliers de charcuterie. 

(e)° L'education du public en ce qui concerne l'emploi des virus des 
rongeurs et le danger possible des viandes crues. 


John C. Torrey, Ph. D., Assistant Professor of Experimental Pathology and 
• Lecturer in Hygiene, Cornell University Medical College, New York City. 

It is generally agreed that our knowledge of the occurrence and 
distribution of the B. enteritidis of Gartner in nature, aside from 
its presence in infected meat, is still far from complete. This bacil- 
lus has frequently been isolated from meat, and, to a less extent, also 
from vegetable foods which have been the causative factors in more 
or less severe outbreaks of food poisoning, but little light has gen- 
erally been shed on the ultimate source of these bacilli nor on the 
mode of infection of the foodstuffs: It is my desire to invite your 
attention to a distributing vehicle for these bacilli which seems to be 
of considerable importance and which has hitherto been entirely 

In the course of an investigation into the etiologv of canine dis- 
temper — an epizootic centering generally in the respiratory tract 
and affecting primarily the mucous surfaces throughout the body — 
I have found that the Bacillus enteritidis (Gartner) is frequently 
encountered in the organs of dogs suffering from this infectious dis- 
ease. This bacillus is not the cause nor even an important factor in 
the disease, but occurs as a more or less sporadic invader of the 


An important symptom of the severer type of canine distemper is 
a bloody mucous diarrhea associated with a more or less intense 
enteritis, and induced primarily by the toxin of the distemper bacil- 
lus (B. bronchisepticus) . On autopsy, the mucosa may be found 
to be eroded and highly congested throughout the large and small 
intestine. It seems probable, accordingly, that the presence of these 
Gartner bacilli in certain organs of the dog is due to their gaining 
access to the lymph or possibly the blood stream through this 
weakened intestinal epithelium. 

In a series of 63 consecutive cases of natural and experimental 
canine distemper, which have been examined carefully bacteriologi- 
cally, the B. enteritidis (Gartner) has been found in one or more of 
the internal organs of 12 dogs, or 19 per cent. As will be presently 
demonstrated, these bacilli are identical with stock cultures of the B. 
enteritidis (Gartner) of definite history and reliable source. These 
bacilli have been encountered most frequently in the liver, next in 
the spleen, and, more rarely, in the kidney, lungs, and blood. In 
some instances only a few colonies of this bacillus haye appeared on 
the plates; whereas, in others, the organs seemed to be swarming 
with them. Such was the finding in a distemper dog which had 
succumbed to a lobular pneumonia. In the consolidated parts of 
the lung the Gartner bacillus was recovered in pure and luxuriant 
culture, while in the unaffected lung areas, and in other organs, there 
were none present. One dog, which had suffered a relapse and was 
very weak, was found to be fairly swarming with the B. enteritidis, 
as it was recovered readily from the blood, the respiratory tract, the 
liver, spleen, and kidney, and in almost pure culture from the large 
and small intestine. 

As a control for these distemper dogs a series of 19 normal dogs 
were examined. The B. enteritidis was found in the organs of only 
one of these and in small numbers in the spleen. Further, the agglu- 
tinins in the blood of this animal indicated that it had only recently 
recovered from an attack of distemper. 

This bacillus apparently does not, as a rule, invade the viscera 
nor multiply in the intestinal tract until the final stages of the 
disease, when the vitality of the animal is seriously impaired by the 
distemper virus, for of the positive findings, 75 per cent occurred 
in animals which were undergoing a severe attack of the disease. 
In this series of 63 cases of distemper there were 28 dogs which were 
either dead at the time of culturing, or were beyond the prospect of 
recovery, and, from the organs of these severe or fatal cases, the B. 
enteritidis was recovered in 9 instances, or in 32 per cent, whereas, 
among 35 dogs which were suffering from mild attacks of distemper, 
or which were autopsied in the early stages of the disease, the 
Gartner bacillus was recovered from only 3, or 8.5 per cent. It 


would seem, then, that about one-third of the dogs which suffer 
severe attacks of distemper are harboring and probably eliminating 
the meat-poisoning bacillus of Gartner. 

In a series of 18 dogs in which material from different portions 
of the intestine was plated out on Endo medium the B. enteritidis 
was isolated in two individuals, or 11 per cent. One of these was an 
animal which had recently recovered from distemper, and the B. en- 
teritidis was found in small numbers in the rectum. The other dog 
was dying from distemper and uncinaria infection. Endo plates, 
seeded with the content of both the small and large intestine, were 
crowded with colonies of B. enteritidis; in fact, this bacillus was 
present in almost pure culture. The blood, and such of the organs 
of this dog as were plated, were also impregnated with large num- 
bers of the bacillus. It is evident that such a case might serve as a 
dangerous distributor of this bacillus. 

This investigation has not been carried far enough to justify a 
definite statement in regard to the frequency of this bacillus in the 
intestinal tract of not only apparently normal dogs, but especially 
dogs dying with distemper, nor have the methods used thus far been 
the most favorable. I believe, however, that a considerable percent- 
age of normal dogs harbor the B. enteritidis in the intestine, although 
in such very small numbers that their isolation is a matter of con- 
siderable difficulty, but during a severe attack of distemper these 
bacilli begin to multiply, and in the last stages may become the 
dominant microorganism in the intestinal flora, as was the case in the 
example just cited. This multiplication is no doubt greatly favored 
by the devitalizing action of the distemper virus, and especially 
by the fact that it may be accompanied by an intense inflammation 
and a very active secretion of mucus by the intestinal epithelium, 
which, as Pies has pointed out, facilitates the growth of bacilli of 
the typhoid group. 

In the course of an investigation into the nature of a destructive 
cheesy pneumonia occurring among laboratory white rats a bacillus 
identical in every way with the B. enteritidis recovered from dogs 
was isolated from the lung of one individual. 

As cats are susceptible to distemper, and also enjoy a natural im- 
munity to the B. enteritidis, it was considered possible that they, 
like dogs, may harbor these bacilli. The results thus far with normal 
cats have been negative. Endo plates made from the liver and spleen 
have always proved sterile, and from the intestinal content no bacilli 
have been isolated which are identical with the meat-poisoning 
bacillus, although types which induce a typical alkalinity in litmus 
milk and ferment glucose with gas production, but not lactose, are 
common, as they are also in the intestinal flora of the dog. None of 
66692— vol 2, pt 1—13 9 


them, however, ferment dulcit, and they failed to agglutinate with 
any paratyphoid serums in dilutions higher than 1-200. They con- 
form to one or more of the types of Morgan's bacillus. The B. proteus 
vulgaris is also common in the intestinal flora of both animals. 

These bacilli isolated from dogs are identical culturally with stock 
cultures of the B. enteritidis (Gartner). They are motile, Gram- 
negative bacilli of typical morphology. They do not produce 
indol in peptone water, but reduce nitrates to nitrites and ferment 
with gas production the carbohydrates, dextrose, levulose, galactose, 
maltose, mannit, dulcit, and sorbit, but not lactose, saccharose, adonit, 
raffinose and inulin. They produce 30 to 50 per cent of gas in dex- 
trose broth, and the Voges-Proskauer reaction is negative. With lit- 
mus milk, the initial acidity gives way in two or three days to an 
increasing alkalinity, which in two to three weeks becomes intense. 

That these cultures isolated from dogs, and also the culture from 
the white rat, are the B. enteritidis of Gartner 5 and not some other 
species of the enteritidis group, is conclusively proved by agglutina- 
tion experiments. The two stock cultures with which they were com- 
pared were obligingly furnished by the department of public health 
of the American Museum of Natural History, New York — one of 
them came originally from the Rockefeller Institute and the other 
from Krai. The culture of B. cholerce suis was received from the 
same source and was originally isolated by Dr. Billings from hog 
cholera. The representative of the paratyphoid B group is a Schott- 
muller strain. The antisera were prepared by inoculating rabbits 

Chart I. 

Identification of B. enteritidis cultures from dogs and rat by agglutination 



1. B. enteritidis, No. 18 (Gartner) 

2. B. enteritidis, No. 132 (Gartner). . . . 

3. Dog baciliua, No. 69, liver 

4. Dog bacillus, No. 82, intestine 

5. Rat bacillus, lung 

6. B. cholerae suis 

7. B. paratyphosus, B. (Schottmuller) 


B. enteri- 

No. 132 


No. 59. 


B. chol- 
erae suis. 








B. para- 


As is shown in the chart the stock cultures of B. enteritidis and the 
dog and rat cultures interagglutinate, whereas none are clumped 
except in very low dilutions by antisera to the B. cholerae suis and 


B. paratyphosus, B. Nor do these two cultures interagglutinate with 
the anti-Z?. enteritidis serum or with the anti-dog-culture serum. 
With a single exception all the cultures isolated from dogs, culturally 
like B. enteritidis, agglutinated with striking uniformity and prac- 
tically to the limit of the serums immune either to the dog cultures 
or to the stock B. enteritidis cultures, and all evidently belong to the 
same strain. In the one exception, the culture isolated from the liver 
of a certain dog agglutinated well, whereas cultures from the spleen, 
although absolutely identical culturally with the B. enteritidis. failed 
both to agglutinate with enteritidis serum and also to absorb any 
specific agglutinin for the same. Stromberg has described similar 
nonagglutinating strains of the B. enteritidis and considers them 
degenerated forms. 

Absorption experiments provide the last link in the proof that 
these cultures isolated from distemper dogs are true representa- 
tives of the B. enteritidis. No attempt was made to exhaust the 
serums in these experiments, but the results show conclusively that 
the dog cultures can absorb the specific agglutinins from an enteritidis 
(Gartner) serum and also that the stock B. enteritidis cultures absorb 
the specific agglutinins from a serum immune to a dog culture. 
Absorptions seem to offer a rational and conclusive mode of identify- 
ing these bacilli of the paratyphoid group, but in many investigations 
have been neglected. 

Strangely enough no specific agglutinins for these bacilli were pro- 
duced in the blood of the dogs which harbored them, although in one 
instance they were found in great abundance throughout the body. 

These cultures from dogs are highly virulent for rabbits, guinea 
pigs, and white mice (as has been reported to be the case with strains 
of the B. enteritidis from other sources), decidedly less toxic for 
white rats and cats, and not at all so for dogs. For guinea pigs they 
revealed a toxicity fully 10 times as great as the stock cultures of 
B. enteritidis (Gartner), 0.001 of a cubic centimeter of a 24-hour 
broth culture proving fatal in 24 hours. Rabbits were killed by 0.1 
cubic centimeter in 24 hours and by 0.01 cubic centimeter in 5 days, 
when inoculated intraperitoneally. One-tenth of an agar culture, 
sterilized by heat, also proved fatal, indicating that the toxin is to a 
certain extent heat resistant, as is known to be the case with Gartner's 
bacillus. White mice are exceedingly susceptible, as 0.001 cubic centi- 
meter of a 24-hour broth culture, inoculated intraperitoneally, killed 
in 24 hours, and 0.0001 in 3 days ; on the other hand, white rats seem 
to enjoy a relative immunity, as about 0.5 cubic centimeter intra- 
peritoneally was required to kill. Two cubic centimeters inoculated 
intraperitoneally into a cat caused a diarrhea and sickness, fatal 
within 14 days. 


In the study of the virulence of bacilli of the enteritidis group, 
feeding experiments are of value and interest. With these dog cul- 
tures I was not successful in inoculating white rats by feeding, but 
with white mice the results were striking and uniformly successful. 
The culture used was a strain isolated from the intestine of a dis- 
temper dog. Mice fed on bread moistened with an emulsion of this 
bacillus sickened in three to five days and died in four to six. days. 
Autopsy showed a congested condition of the small intestine and a 
bloody mucous content, the spleen was much swollen and dark, and 
the liver embodied more or less extensive and scattered necrotic areas ; 
there appeared also in certain instances a congested state of the lungs, 
with some consolidation. Pure cultures of these bacilli were recov- 
ered from the heart blood, the liver, and the spleen. 

As is well known, the B. enteritidis (Gartner) is not toxic for the 
dog, and the enteritidis cultures isolated from the dogs themselves 
proved no exception to this rule. A puppy withstood the intra- 
peritoneal inoculation of several thousand times the fatal dose for 
rabbits without ill effect. The subcutaneous inoculation of large 
doses of this bacillus produced a more or less extensive gaseous swell- 
ing, but the animal seemed to suffer little, if any, (Jiscomfort. This 
tolerance of the dog to the meat-poisoning bacillus seems of consid- 
erable importance, as it permits a great increase of the bacilli within 
the body and a long period of elimination before death from dis- 
temper ensues. 

As far as I am aware, there is no record in the literature of the B. 
enteritidis (Gartner) being isolated from dogs. Although members 
of the intermediate group have been reported as occurring in these 
animals, yet the identification has not been definite. Ruediger, in 
the Philippines, has reported the isolation of a paratyphoidlike 
bacillus from the blood and organs of a dog examined for Negri 
bodies. This bacillus was culturally like the intermediate group, 
but its specific affinities could not be determined by agglutination — 
no enteritidis serum was available. Courmont and Rochaix, also 
Vallet and Reinbaud, have described intermediates as occurring with 
more or less frequency in the fecal discharges of dogs, especially those 
of the street. These bacilli were not specifically identified, however, 
and, from the descriptions, many were atypical B. coli. Aside from 
these reports, the importance of the dog as a distributor of bacilli 
of the paracolon group has never been realized. Bacilli of this 
group have occasionally been reported as associated with epizootics 
among guinea pigs and rabbits in various parts of the world. 
O'Brien and Petrie recovered the B. mipestifer from victims of one 
outbreak, and Bainbridge and O'Brien the B. enteritidis from an- 
other. Boycott has described an infective methemoglobinuria oc- 


curring naturally among white rats, caused by the B. enteritidis, and 
prevailing to the extent of 1 per cent of the total number. Rat 
viruses are commonly prepared with strains of the B. ententidis and 
this bacillus may be more or less widely distributed through these 
animals. This bacillus, or nearly related ones, have been described 
as the cause of enteritis in a considerable variety of birds and mam- 
mals other than those already specified. 

Granting that these strains of the B. enteritidis, which occur under 
varying conditions in animals, may possess infective properties for 
man — and, although there is not sufficent evidence for generalization, 
in certain instances they have been proved to possess such a char- 
acter — the dog apparently presents the greatest source of danger as 
a distributor of the meat-poisoning bacillus of any of the domestic 
animals, coming, as it does, in close and generally almost unrestricted 
contact with man and his food products. It is noteworthy that dis- 
temper is exceedingly common among young dogs, and that a very 
high percentage of street dogs suffer from the infection during the 
first years of life, with a death rate of 30 per cent, or higher. Dogs 
are very commonly kept by farmers and dairymen, and generally 
have free access to the stockyards and stalls of the cattle. A certain 
proportion of them inevitably suffer from an attack of distemper, 
and it is quite possible that they are at times in a position to infect 
live stock with the Gartner bacillus, either directly, or indirectly 
through their food, and also the milk. 

It may also be the case that certain of the obscure cases of food 
poisoning, especially those which have been induced through the 
consumption of infected vegetable foods, may have their ultimate 
explanation in the contact of distemper dogs with such commodities. 

The obvious conclusion from these findings is that it is safer to 
exclude carefully dogs suffering with distemper from all possible 
contact with food and live stock, and it should be borne in mind that 
the danger from these animals as the eliminators of the B. enteritidis 
increases as death approaches. 


Dr. P. G. Heinemann, Department of Bacteriology, University of Chicago, 111. 

This investigation was carried on with the object of determining 
whether a reliable indicator of methods of producing milk could be 
found. The samples were bought in the open market in original 
packages; 215 samples were examined. Of this number, 108 samples 
were raw milk, and 107 samples pasteurized milk. The samples were 


carried to the laboratory packed in ice and examined immediately 
after arrival. The following determinations were made: 

1. The amount of dirt was ascertained by the method described by 
Torrey. 1 The results were expressed in milligrams per liter. 

2. Counts of colonies per cubic centimeter of milk were made and 
the acid colonies counted separately. 

3. The number of bacteria of the B. coli group in 10 cubic centi- 
meters of milk was determined by inoculating 1 cubic centimeter and 
0.1 cubic centimeter of milk each in five fermentation tubes containing 
1 per cent dextrose infusion broth. 

4. The number of aerobic spores was determined by inoculation of 
1 and 0.1 cubic centimeters milk each in five tubes of litmus milk, and 
the tubes heated to 85° C. for 15 minutes. 

5. The number of anaerobic spores was determined by inoculation 
of 1 and 0.1 cubic centimeters of milk each in five tubes of litmus 
milk. The tubes of litmus milk were heated to the boiling point 
previous to inoculation and after inoculation heated to 85° C. for 15 
minutes. The surface of the milk was then covered with a layer of 
mineral oil, previously sterilized by boiling. 

A summary of the results of this investigation leads to the assump- 
tion of the following facts : 

1. The average number of colonies per cubic centimeter in 108 
samples of raw milk was 4,801,300, in 107 samples pasteurized milk, 

2. The percentage of acid colonies in raw milk was 31, and in 
pasteurized milk, 28. 

3. The average number of bacteria of the B. coli group in 10 cubic 
centimeters raw milk was 14; in 10 cubic centimeters pasteurized 
milk, 19. 

4. The average number of aerobic spores in 10 cubic centimeters 
raw milk was 47 ; in 10 cubic centimeters pasteurized milk, 63. 

5. The average number of anaerobic spores in 10 cubic centimeters 
raw milk was 46; in 10 cubic centimeters pasteurized milk, 61. 

6. The average number if milligrams dirt per liter of raw milk 
was 2.2 ; of pasteurized milk, 1.4. 

I conclude from these results that : 

1. Commercially pasteurized milk turns sour the same as raw milk, 
and that there is no consistent relation between acid colonies and 
the total number of colonies. 

2. Pasteurized milk contained less dirt than raw milk. The pro- 
portion was as 11 for raw milk to 7 of pasteurized milk. The method 
employed shows, however, the insoluble dirt only. 

3. The relation of the number of bacteria of the B. coli group in 
raw milk to the number in pasteurized milk was as 9.5 to 7. This 
shows that either some of the milk sold as pasteurized was not effi- 


ciently pasteurized, or that there are some highly resistent forms of 
B. coli which survive pasteurization. 

4. The relation of the number of aerobic spores in raw milk to the 
number in pasteurized milk was as 3 to 4. 

5. The relation of the number of anaerobic spores in raw milk to 
the number in pasteurized milk was as 3 to 4. 

6. There was no relation between the number of bacteria of the 
B. coli group, or of the aerobic spores and anaerobic spores to the 
total number of bacteria or to the acid colonies. 

7. The temperature of milk during transportation is a variable 
factor, and the relation of groups of bacteria in milk is probably 
shifted by multiplication. The results obtained in this investigation 
can therefore have no bearing on the relation of groups of bacteria 
in freshly drawn milk. 

8. Total counts seem to be the only means of judging methods of 
production and transportation. By this method we can not dis- 
tinguish definitely between methods of production and transporta- 
tion. However, a large proportion of acid colonies, accompanied by 
a small amount of dirt, would indicate faulty transportation, and a 
small proportion of acid colonies and a large amount of dirt would 
indicate faulty production. When both production and transporta- 
tion are faulty, one may expect to find large total numbers, a large 
number of acid colonies, and a large amount of dirt. By making 
these three tests a fairly accurate insight into the quality of the milk 
may be obtained. 

'Amer. Jour, of Public Health, 1912, vol. 2, p. 280. 

Dr. W. H. Park : There are only two points upon which I can not 
quite agree with the paper of Dr. Henderson Smith, and I wish to 
comment upon these. He has concluded that the dysentery types 
other than Shiga are not constant, and that the absorption agglu- 
tination test is not of great value in differentiating the different 
stains. In the United States the workers have found that the maltose- 
fermenting type and the manite- fermenting type are equally stable 
and distinct, and with the more important Shiga type are the excit- 
ing factor in the great majority of cases of dysentery. The small 
percentage of cases remaining seems to be due to quite a number of 
other varieties. In Germany also, I believe, it is recognized that these 
groups exist. The cultures obtained by Hiss, myself, and others have 
in cultural and agglutination test fallen into these groups and con- 
tinued true in their characteristics. In a broad sense this is proba- 
bly true throughout the world, although in special localities bacilli 
of different characteristics may predominate. I believe in patho- 


genie varieties of bacteria the agglutination characteristics are as 
important as fermentation characteristics. 

Dr. W. Fornet, Berlin, gibt Herrn Smith darin Recht, dass ein 
grosser Teil der bei der Differenzierung von Para typhus- und para- 
typhusahnlichen Bazillen entstandenen Schwierigkeiten dadurch 
vermieden worden ware, wenn alle Untersucher nur sichere Para- 
typhusbazillen als Vergleichsobjekte benutzt hatten. Dies ist nicht 
der Fall. Beschrankt man sich darauf, zunachst nur solche Bazillen 
mit entsprechenden kulturellen und biologischen Eigenschaften als 
Paratyphusbazillen zu bezeichnen, die aus dem Blut von paratyphus- 
kranken Menschen geziichtet waren. Unter Beobachtung dieser 
Vorsichtsmassregel ist es mir immer gelungen, mittels der Absortions- 
methode nach Castellani den Paratyphus B. Bazillus von alien ahn- 
iichen mit Sicherheit zu unterscheiden. 

Herr Kollege Smith vom Lister Institut hat den Vorschlag 
gemacht, eine Kommission zu ernennen, die eine einheitliche Unter- 
suchungsmethode fur die Typhus-Coligruppe ausarbeiten soil. 
Dieser Vorschlag ist unterstiitzt worden von Herrn President Welch 
und H. Stabsarzt Fornet und ich selbst habe in meinem Referat auf 
die Notwendigkeit, sich erst iiber eine einheitliche Untersuchungs- 
methode zu einigen, hingewiesen. Es ist dies der erste Schritt den 
wir thun mussen, um Klarheit in die verworrene Frage zu bringen. 
Ich mochte mir nun erlauben, gleich einige Vorschlage fur die Zusam- 
mensetzung dieser Kommission zu machen, die natiirlich ganz unmass- 
geblich sein sollen. 

Iche mochte vorschlagen in erster Linie unsern verehrten Vorsit- 
zenden Herrn Prof. Theobald Smith, Herrn Direktor Park und Herrn 
Kollegen Winslow, ferner das Lister Institut in London, H. Kol- 
legen Smith, das Institut Pasteur in Paris, das Hygienische Institut 
der Universitat Wien, Prof. Babes aus Bukarest, das Hygienische 
Institut der Universitat Greifswald (Loeffler), das Institut fur In- 
fektionskrankheiten Robert Koch (Berlin) und das Kaiserliche 
Gesundheitsamt Berlin. 

Es ist nun aber immer so eine Sache mit solchen iiber die Erde 
zerstreuten Kommissionen, ihre Tatigkeit und Wirksamkeit ist 
erschwert, ja in Frage gestellt, wenn nicht eine Centrale vorhanden 
ist, welche die Initiative ubernimmt und die Verbindung mit den 
verschiedenen Mitgliedern aufrecht erhalt, Sie hatte im vorliegen- 
den Fall vielleicht auch den ersten Entwurf zu einem Plan fiir eine 
einseitliche Untersuchungsmethode der Typhus-Coligruppe aufzu- 
stellen und den andern Mitgliedern zur Ausserung zuzusenden. 
Vielleicht wiirden die amerikanischen Kollegen diese Centrale bilden. 

Dr. E. Libman, Mount Sinai Hospital, New York: In much of 
the work done in recent years, an important fact has been lost sight 
of — that it is essential to use optimum media for determination and 


production, a point emphasized many years ago by Durham. Most 
of the media now used are not sufficiently favorable, especially when 
one is dealing with organisms that grow well. In an extensive re- 
search made by Drs. Celler and Sophian and myself, in the labora- 
tories of the Mount Sinai Hospital, it was found that agar plus 
carbohydrates was a most unfavorable medium for detection of acid 
production. And still that medium is most used. The next best 
medium is bouillon plus the carbohydrates. Still more favorable are 
agar media with serum and carbohydrates (we used ascitic serum). 
But the best media are made up from bouillon by the addition of 
serum and the various carbohydrates. I believe that a still better 
medium can be made up. 

For a number of years the serum-water media have been much em- 
ployed, both here and abroad. Hanna, in 1908, introduced a medium 
consisting of water 9 parts and ox serum 1 part : with carbohydrates 
and litmus. Hiss, a few years later, advised the use of a similar 
medium, but containing 2 parts of water and 1 of serum. 

In 1905 Dr. Buerger advised the addition of 1 per cent of peptone 
to the last-mentioned serum- water medium. This medium is far 
superior to that made up without peptone, but is not quite as good as 
the media made up of bouillon serum and carbohydrates. 

When our complete studies are published it will also be made clear 
that titre is important. Growth may be very poor in a medium with- 
out serum at a certain titre, and much better with serum at another 
titre. If optimum media will be more used by investigators than they 
are at present, it is very probable that we shall find less variants than 
are now believed to exist. 

C. E. A. Winslow, New York : I have listened with great pleasure 
to these papers and particularly to the admirable treatment of the 
subject of variability by Dr. Smith. The investigations of the last 
few years, in which the workers at the Lister Institute have played a 
leading part, have made it clear that bacteria do vary, particularly 
when exposed to certain definite environments. If these variations 
are considered from a broad biological viewpoint, however, they offer 
no serious obstacle to scientific classification. 

In the first place, the variations which occur, so far as carbohydrate 
fermentation is concerned^ are of a definite and orderly character. 
We have worked this out in the case of the streptococci and have 
found that the sugars stand in a pretty regular order of availability. 
The monosaccharide, dextrose, is most easily attached. Then come 
the disaccharides, lactose, and saccharose and the glucoside, salicin. 
Raffinose is more difficultly utilizable and inulin and mannite still 
more so. There are exceptions to every rule in biology, but in gen- 
eral we find that streptococci which attack inulin and mannite can 
attack all the simpler carbohydrates, those which ferment raffinose 



ferment the disaccharides, and those which ferment the disaccharides 
all utilize dextrose. The term " metabolic gradient " has been ap- 
plied to this relationship and the differences between relationship and 
the differences between streptococci, according to this conception, are 
not haphazard, but consist in the addition or subtraction of a series 
of enzymes, each of which, superposed on the rest, makes available 
a new and more couple- carbohydrate. • 

In the colon group, it is interesting to note that the metabolic 
gradient is quite a different one. It is the size of the molecule which 
mainly controls assimilation with the streptococci. Those that at- 
tack lactose almost always attack saccharose equally well. The colon 
group, on the other hand, all break up lactose but only half of them 
ferment saccharose, and those that do can break up rafnnose equally 
well. Here it is the configuration of the molecule not its size which 
determines availability. Aldehydic sugars are assimilated by all, 
while only one subgroup can ferment ketonic sugars. To those that 
have the latter power, the size of the molecule appears to be 

The practical difficulty we have to meet in classification is that 
offered by minutely integrading forms. Certain workers in England 
and in this country have come to the conclusion that there is just 
one way out of the dilemma of big heterogeneous groups on the one 
hand and innumerable varietal names or numbers on the other. That 
is the use of the statistical or biometric method. If you measure quan- 
titatively the important characters of a considerable series of bacteria 
belonging to a group and plot them, you find that they group them- 
selves naturally about certain modal points or centers of variation. 
To these type centers, about which the individual strains are varying, 
we can conveniently give specific names, regarding the rarer forms 
between as simply variants from the central types. By such a study 
of populations, rather than individuals, the relations of the puzzling 
group of the cocci have, I think, been made clearer than they were 
before, and more recently Dr. Howe and Dr. Morse, both of 
Boston, have applied the same methods to the colon group and the 
diphtheria group, respectively, with marked success. I may say, in 
passing, that so far as the colon group is concerned, Dr. Howe has 
in the main brought us back to the simple division into saccharose 
fermenters and nonsaccharose fermenters, which was pointed out by 
our chairman, Dr. Theobald Smith, so many years ago. 

It does not in the least detract from the value of a statistical 
classification to say that under changing conditions the properties of 
the bacteria may change as well. As the populations of bacteria 
exist in nature, they do group themselves about definite type centers, 
which are perhaps habitat species molded to some extent by the 
conditions surround in# them, but real entities nevertheless, and the 


only practical units which we have for the identification and cla 
fication of bacterial forms. 

Dr. William H. Welch, Baltimore, Md. : In view of the confu- 
sion relating to the classification and differentiation of the so-called 
paratyphoid or intermediate group and of the great inequalities in 
the methods of studying this group I would suggest the desira- 
bility of appointing, with the approval of this congress, an inter- 
national commission to consider the methods of investigation of 
bacteria of the Colon-typhoid group with a view of reaching an 
agreement at least as to the more essential tests which should be 
employed in the study and description of members of the group. 
Such a commission could perhaps report to the next congress, but it 
would be desirable to publish their conclusions as soon as formu- 
lated. This proposal is one which may perhaps be considered at the 
end of this meeting. 


Nestor Morales, delegado de Bolivia ante el XV. Congreso Internacional de 
Higiene y Demograffa en Washington. 

He creido que seria de importancia para vosotros el conocer un 
aspecto aun no estudiado de la tuberculosis, cual es el que se refiere 
a la tuberculosis experimental en las grandes alturas. 

El hecho es tanto mas importante, cuanto que mientras en Europa 
ya a los 4,000 metros sobre el nivel del mar, existen las nieves eternas 
y la vida humana es casi imposible ; en mi pais existen a alturas que 
varian de 3,000 a 4,000 metros poblaciones florecientes, que tienen 
de 20,000 hasta 100,000 habitantes. 


Sabemos cuales son las condiciones que facilitan la propagacion y 
desarrollo del bacilo de Koch ; entre estas tenemos en primer termino 
el aire confinado, la miseria y un elevado grado higrometrico ; es por 
esta razon que en las grandes capitales del Vie jo Mundo, es donde la 
tuberculosis hace particular destrozo, mientras que las pequeilas 
poblaciones rurales y los habitantes del campo, son mucho menos 

Sentado el principio que antecede, es facil comprender que en las 
poblaciones bolivianas, donde la miseria es casi desconocida y en las 
cuales la aglomeracion urbana es insignificante, y cuyo aire es cons- 
tantemente calentado por un sol que no cesa de brillar en todo el ano, 
la tuberculosis haya sido rara y quiza no haya existido, sino en epoca 
muy posterior. 

Consultando las paginas de la histpria medica de mi pais, y muy 
especialmente del Departamento de La Paz, he obtenido la firme con- 


viccion de que hasta el ano 1880 la bacilosis era desconocida. Poco 
tiempo despues, el movimiento comercial y las inmensas riquezas 
minerales del suelo boliviano, atrajeron una corriente de inmigracion, 
cuyos primeros representantes fueron los trabaj adores peruanos y 
chilenos de la costa del Pacifico, y junto con ellos vinieron a medi- 
cinarse los primeros tuberculosos, atraidos por la belleza del clima y 
la accion saludable de la altura. 

La Paz, poblacion que cuenta en el momento actual con 100,000 
habitantes, poco mas 6 menos, esta situada a los 16° 29' 30" de latitud 
y a los 70° 19' 40" de longitud. siendo su altura de 3,(565 metros. Su 
clima es benigno, siendo las temperaturas medias en verano y en 
invierno mui soportables; de manera que los calores sofocantes asi 
como los excesivos frios, son absolutamente desconcidos. 

Se comprende pues, que las favorables condiciones del clima 
fueran debidamente apreciadas por los enfermos, muchos de los cuales 
curaron en condiciones sum anient e satisf actorias, y los cuales al volver 
a su patria, ponderaron las inmejorables condiciones del clima de La 
Paz, lo que logicamente atrajo una cantidad considerable de enfermos. 

A partir de los afios 1886 y 1887, se empezaron a observar los 
primeros casos de tuberculosis indigena, y lo que es digno de llamar 
la atencion, con un caraeter de extraordinaria gravedad, como si el 
bacilo de Koch hubiese, al encontrar un terreno esencialmente nuevo^ 
exaltado su virulencia, hasta el punto de que las bacilosis aqui observa- 
das han tenido siempre una marcha subaguda y rapidamente mortal. 

Otro hecho sobre el que me permito llamar la atencon de este ilustre 
Congreso, es que la tuberculosis ha manifestado particular predilec- 
cion por la raza indigena^ en la que se ha presentado con mucha mayor 
frecuencia que en la blanca 6 mestiza. 

La extrana marcha de la enfermedad, asi como la circunstancia de 
que todos 6 la mayor parte de los que venian de la costa se curaban en 
breve plazo, hacia importante el estudio bacteriologico experimental 
del bacilo de Koch, para darse cuenta exacta de las particularidades 
que ofrecia a la observacion. Es respondiendo a esta necesidad, que 
el ano proximo pasado empeze un estudio minucioso sobre la tubercu- 
losis experimental en las grandes alturas. 


Con el proposito de dar la mayor amplitud posible a las investiga- 
ciones, me diriji, de una manera oficial a los siguientes institutos, 
para que se sirvieran procurarme culturas puras de bacilo tuberculoso : 

Tnstituto de Bacteriologia del Departamento de Agricultura de 
Norte America, Instituto Pasteur de Paris, Instituto Real de Viena, 
Instituto de Higiene de Santiago de Chile, Instituto de Higiene de la 
Republica Argentina. 


Las culturas se recibieron sucesivamente y este fue el resultado de 
las primeras investigaciones : 

Culturas norteamericanas. — Se recibieron en fecha 10 de enero 
del ano en curso, e inmediatamente se procedio a hacer una inocula- 
cion subcutanea en un cobayo de 300 gramos. 

Observadas las temperaturas en la manana y en la tarde, no se noto 
modificacion apreciable, a excepcion de un ligero aumento durante la 
tarde del primer dia. 

La reaccion local se redujo a una pequena induracion en el punto 
inoculado, y al infarto ganglionar de los ganglios inguinales, infarto 
que en la segunda semana desaparecio por completo. habiendo desde 
entonces el cobayo recobrado la salud. El peso disminuyo 10 gramos 
durante la primera quincena; pero luego volvio a elevarse hasta 
llegar a 400 gramos, sin que el animal volviera a presentar sintoma 
de ninguna especie, Seis meses despes, el animal continuo con- 
servando un apetito excelente y una salud buena. 

Cobayo No. 2. — Cultura de bacilo tuberculoso procedente de Viena 5 
infectada de hongos. Yiendo el resultado negativo de las primeras 
experiencias, pense que probablemente la pequena cantidad de bacilos 
inyectados en el primer caso habria sido insuficiente para determinar 
el proceso patologico de experimentacion, y es por esta razon que, en 
esta segunda experiencia, se tomo una considerable cantidad de la 
cultura habiendose inyectado en el peritoneo 2 centimetros cubicos de 
una emulsion concentrada de bacilo de Koch. Las experiencias em- 
pezaron el 14 de marzo, con un cobayo cuyo peso era de 415 gramos 
en el momento de la operacion. Dos meses despues, como el animal 
no diera muestra de sufrir en lo mas minimo, sino que el peso se habia 
elevado a 475, se resolvio sacrificar al animal, para ver si existian 6 
no en su organismo focos profundos de bacilosis de marcha cronica. 

Verificada la autopsia, no se econtro un solo bacilo, y las culturas 
que se hicieron en suero glicerinado quedaron esteriles. 

Cobayo No. 3. — Cultura procedente del Instituto Pasteur de Paris. 
Cobayo de 420 gramos, inoculado en fecha 28 de febrero con 2 centi- 
metros cubicos de emulsion concentrada. En la tarde, elevacion de 


temperatura a 39°, siendo la temperatura normal de los cobayos en 
esta altura 38° 6'. El animal esta abatido, ha tornado poco alimento, 
lo que prueba que hay una accion toxi-infecciosa energica sobre su 
organismo. Al dia siguiente, la temperatura ha vuelto al tipo nor- 
mal, el apetito reaparece sin que el animal de prueba de sufrir nada. 
Ocho dias despues, examinando los ganglios se puede notar un ligero 
infarto, el que va desapareciendo rapidamente, de manera que seis 
meses despues el animal tiene 40 gramos de aumento en su peso y 
un estado de sanidad completa. 

Cobayo No. 4- — Cultura del Instituto de Higiene de Chile. Cobayo 
de 435 gramos de peso, inoculacion subcutanea, el 19 de abril, con 


2 centimetros cubicos de emulsion concentrada. La reaccion es nula. 
Pasados veinte dias, se present a un pun to indurado en lugar de la 
inoculacion, el que se reblandece y da lugar a la produccion de un 
pequerio absceso, en cuyo pus se pueden distinguir muy pocos bacilos. 
Sembrado el pus, tan to en suero glicerinado cuanto en geleosa glice- 
rinada, no determina la produccion de cultura. El animal pierde 15 
gramos de su peso ; pero a los ocho dias, cicatrizada la pequeiia 8 lu- 
ceracion, el peso aumenta llegando a 478 gramos. 

Cuatro meses despues, se comprueba un estado completo de sanidad 
en el cobayo. 

En el caso anterior es indudable que se trataba de un proceso local 
de bacilosis, que no ha llegado a generalizarse, debido a la reaccion 
defensiva del organismo. 

Cobayo No. 5. — Cultura procedente de la Kepiiblica Argentina. 
Peso de 460 gramos. Inoculado en fecha 20 de febrero con 2 centi- 
metros cubicos de emulsion concentrada. Resultado negativo. No 
habiendose presentado reaccion apreciable en ninguna forma. 

Por la relacion que antecede, se ve que las culturas de diferente 
procedencia, inoculadas sea en forma subcutanea 6 intra-peritoneal, 
han dado un resultado constantemente negativo. Habiendose limi- 
tado las manifestaciones de defensa organica a fenomenos de po- 
quisima importancia, los mismos que desaparecieron en corto plazo. 

La interpretacion de este fenomeno puede ser multiple, y para la 
claridad de la exposicion le dividiremos en tres grupos: 

1°. Las culturas, a causa de un largo viaje, habian envejecido? Es 
decir, perdido sus primitivas propiedades, para convertirse en ele- 
mentos inertes. 

2°. El aumento de globulizacion en las grandes alturas, hecho com- 
probado por los estudios de Vergara Lope y de Viault, habian de- 
terminado una mayor potencia de reaccion organica, y por con- 
siguiente los elementos defensivos siendo en mayor numero habian 
provocado una destruccion del elemento microbiano? 

3°. Las culturas al llegar a un clima distinto del que habian vivido 
habian, en contacto de un medio nosologico estrano r habian perdido 
sus primitivas propiedades? 

Estas serian las tres maneras de explicar el fenomeno observado 
con la inoculacion de las culturas extrangeras. 

La primera explicacion no me parece plausible ; pues, las resiembras 
dieron nacimiento a nuevas colonias, aunque en numero menor y, por 
otra parte, es sabido que el bacilo tuberculoso, aun en contacto del 
aire y de la luz, elementos que le son absolutamente contrarios, 
guarda su virulencia durante un tiempo mucho mayor que el que 
tardaron las culturas en llegar a la ciudad de La Paz, algunas de las 
cuales, como las procedentes de la Argentina y Chile, solo demoraron 
de 16 a 20 dias. 


La segunda explicacion, que consiste en la mayor defensa organica 
fagocitaria, dependiente de la hiperglobulizacion, tampoco me parecc 
satisfactoria, tanto mas, cuanto que el papel defensive de los fago- 
citos ha perdido una parte de su valor, con los nuevos estudios del 
Profesor Ehrlich. 

Nos queda, para explicar el fenomeno estudiado, la accion del 
medio nosologico, la que a mi juicio tiene may ores probabilidades de 

Efectivamente, sea que consideremos a las bacterias como a algas 
microscopicas anaclorofilianas, sea que en ellas veamos organismos 
de la escala zoologica inferior, el hecho es que, vegetales 6 colocados 
en la serie animal, es indudable que sufren como todo ser organizado, 
la accion del medio ambiente, que en ciertas ocasiones les esteriliza 
por completo quitandoles su potencia reproductora. 

No necesito mencionar muchos ejemplos ante esta ilustre asamblea, 
me bastard citar la falta de reproduccion de los animales africanos 
en el medio europeo, y la falta completa de desarrollo de los vegetales 
de la zona tropical americana, en los climas frios del norte 6 del sur 
del continente. 

Pero aun debo dar a conocer otras experiencias, que a mi jucio son 
absolutamente convincentes, una vez que demuestran con certi- 
dumbre completa la afirmacion que acabo de sentar. 

He dicho que la tuberculosis importada se cura en este clima de 
altura; he dicho tambien que la tuberculosis indigena tiene una 
marcha esencialmente grave. Traduciendo con otras palabras, pode- 
mos decir que el bacilo no aclimatado muere y que el bacilo que ha 
tornado carta de ciudadania es eminentemente temible por su excep- 
cional virulencia. 

Las experiencias siguientes nos parecen particularmente intere- 
santes : 

Cobayo No. IB (peso, 600 gramos). — Inoculado el 11 de julio de 
1911 con esputo tuberculoso, procedente de un individuo de la costa de 
Chile, presentando gran cantidad be bacilos al examen microscopico. 
Falta completa de temperatura; quince dias despues ligera tumef ac- 
cion en el punto inoculado, a los seis dias se forma un pequeno abs- 
ceso que se abre fuera, dando salida a un pus espeso, en el que se des- 
cubren bacilos de Koch. El peso no ha disminuido, el animal con- 
serva un apetito satisf actorio ; el 5 de agosto la herida ha cicatrizado 
por completo, el animal aumenta de peso. Conclusion: tuberculosis 
localizada, que termina por la curacion. 

Cobayo No. 2B. — Inoculado el 10 de octubre de 1911, con esputo 
tuberculoso comprobado por el examen microscopico. Peso, 540 
gramos en el momento de la operacion. El esputo provenfa de una 
persona de la costa de Chile, que habia venido a medicinarse a la 
ciudad de La Paz. 


Los dias siguientes, el animal solo demuestra un ligero aumento 
de 5 centigrados en su temperatura ordinaria, hipertermia que des- 
aparece al octavo dia. No hay reaccion local. Tres meses despues 
el animal ha aumentado 15 gramos de peso. El apetito y la salud 
general se conservan en condiciones satisfactorias. 

Cobayo No. SB. — Inoculado en 12 de octubre de 1911. Inoculacion 
intraperitoneal, esputo comprobado tuberculoso por examen miscros- 
copico, enfermo procedente de Chile. El 22 del mismo mes, eleva- 
cion de temperatura a 39° ; el cobayo esta abatido y triste, los pelos 
levantados, el apetito nulo. Este estado se cOnserva durante ocho 
dias, al cabo de los cuales el animal vuelve a recobrar el apetito, el 
peso que habia disminuido en 50 gramos, empieza a elevarse nueva- 
mente. Cuatro meses despues el animal se encuentra completamente 

Llamo la atencion sobre el hecho de que en esta serie de experien- 
cias, que no quiero continuar detallandolas, pues siempre en todas 
las inoculaciones se obtuvo identico resultado, el esputo que se empleo 
siempre procedia de personas de la costa de Chile; es decir, eran 
como les he calificado bacilos extrangeros. 

Ahora voy a tomar de los muchos estudios que se hicieron, algunos 
ejemplos de la marcha experimental de la tuberculosis contraida en 
La Paz. 

Cobayo No. 1G. — Inoculado con esputo tuberculoso comprobado 
por examen microscopio, procedente de un individuo joven que 
habia contraido la enfermedad en esta ciudad. Peso en el momento 
de la inoculacion, 950 gramos. Fecha de la inoculacion, Julio 16, 
1912; horas, 10 a. m. 

Durante los primeros ocho dias el animal no parece sufrir, pero 
desde esta fecha la temperatura se eleva, sobretodo en la tarde, 
llegando a 39° 4' a 39° 5 r ; el apetito disminuye rapidamente, se pre- 
sentan deposiciones diarreicas. El animal se queja y cuando se le 
toca la region abdominal, se comprueba un grado de sensibilidad 

El 8 de agosto el peso ha disminuido a 750 gramos. Muere 
el 18 del mismo mes, presentando el abdomen enormemente aumentado 
de volumen. 

En la autopsia se constata en el peritoneo un derrame sero-purulento 
muy abundante y de mal olor ; las paredes peritoneales estan cubier- 
tas, en toda su extension, de una capa de peritonitis exudativa. Los 
intestinos repletos de gases se hallan banados de un liquido puru- 
lento; en la gran curbadura del estomago se encuentra un foco de 
>upuracion que forma un verdadero absceso. 

Examinados los diferentes exudados, se ve que encierran bacilo de 
Koch en gran abundancia. 




Cohayo No. 2G (peso, 500 gramos). — Inoculado con esputo prove- 
niente de un indfgena de 15 afios, hecha el 25 de Julio de 1012. Hasta 
el 4 de agosto no se nota ningnna modification apreciable, pero desde 
esta fecha la temperatura se eleva ligeramente en la tarde y el peso 
comienza a disminuir de manera que en agosto 12 solo da 410 gramos. 
Muere el 18 de este mes. A la autopsia se encuentran en el peritoneo 
abundantes granulaciones; el hfgado aumentado de volumen esta tam- 
bien sembrado de granulaciones, que le dan un aspecto grisaceo; los 
pulmones disminuidos de volumen, casi exangiies, contienen numero- 
sas granulaciones y hasta focos de degeneration. 

Las dos experiencias anteriores, tomadas como las mas importantes 
entre varias otras, nos dan la prueba de que es indudable que el bacilo 
tuberculoso indfgena es mucho mas virulento que el importado ; pues, 
si se compara la primera, segunda y tercera serie de experiencias, se 
ve que la primera y la segunda, en las que se ha empleado sea cul- 
turas puras 6 esputos con bacilo extrangero, en todos ellos la curacion 
se ha producido, en plazo mas 6 menos breve; mientras que las in- 
oculaciones llevadas a cabo con esputos conteniendo bacilo indfgena 
han producido la muerte en espacio de tiempo relativamente corto. 

6 Como explicar este fenomeno? No quiero cansar la atencion de 
esta ilustre asamblea, con la exposition de largas teorfas, y es por esta 
razon que me voy a limitar a exponer en pocas palabras, cual es en mi 
concepto la explication del hecho observado. 

Como ya en otro punto he dicho, yo creo que tanto las culturas como 
los esputos con bacilo extrangero no se encuentran aclimatados, de 
suerte que su action es casi ineficiaz y, por otra parte, como pasa con 
todo organismo que no se encuentre en su verdadero medio, la repro- 
duction es nula; de aquf es facil deducir que debilitados los bacilos 
por una parte y no reproduciendose por otra, la economfa se encuen- 
tra en condiciones muy favorables, para reparar todos los danos 
causados por la enfermedad. 

Cosa muy diferente pasa con el bacilo que ya ha tornado carta de 
ciudadanfa en estas alturas; en este caso el bacilo esta aclimatado, y 
como encuentra un terreno nuevo, es facil tambien explicarse la razon 
de su particular virulencia. 

La Paz, Agosto de 1912. 

Temperaturas medias, mdximas y minimas, 190 If. 


Media de 


y minima. 

Media de 

las maxi- 


Media de 
las minimas 











En junio la media maxima viene a ser 17.S; media minima, 0.^. 
En julio hemos tenido media maxima 15.5; media minima, :?.^. 

66692— vol 2, pt 1—13- 



Dr. Georg Becker, Plauen i. Vogtland. 

Von dem friiher allgemein iiblichen radikalen chirurgischen Vor- 
gehen bei der Milzbrandpustel des Menschen ist man in letzten 
Jahren fast allseitig zuruckgekommen. Zwar wird von einzelnen 
Forschern noch einem energischen aktiven Eingreifen das Wort 
geredet, so empfiehlt Barlach (Neumiinster) eine kreisformige Kau- 
therisation um die Pustel und Jodeinspritzungen in der Umgebung, 
Graf (Frankenhausen) friihzeitige Aetzung der Pustel mit dem 
Kalistift, doch ist die Exzision der Pustel weit im Gesunden, even- 
tuell mit Ausraumung der regionaren Lymphdriisen wohl nur noch 
wenig in Anwendung. Auch im Hamburg-Eppendorfer Kranken- 
haus ist die friiher geiibte aktive Therapie seit 1896 verlassen worden 
zu gunsten eines streng konservativen Verhaltens mit Enthaltung 
von jeglichem Eingriff. Das seitdem bis zum November 1911 so 
behandelte Material von 60 Fallen ist von mir in den Mitteilungen 
aus dem Hamburgischen Staatskrankenanstalten, Bd. XIII, Heft 2, 
ausftihrlich veroffentlicht. 

Bei der Bewertung der Therapie hat sich die bakteriologische 
Untersuchung des Blutes sehr bewahrt. 

Die Anwesenheit der Milzbrandbazillen im- Blut ist leicht nach- 
zuweisen, wenn man das mit einer Luerschen Spritze aus der Arm- 
vene entnommene Blut direkt in verflussigten und auf 40-45° abge- 
kiihlten Agar verimpft; auf den dann in Petrischalen ausgegossenen 
Nahhrboden entwickeln sich nach 12-24 stiindigem Aufenthalt im 
Brutschrank die charakteristischen Kolonien. 

Die in 45 Fallen vorgenommene bakteriologische Untersuchung 
des Blutes ergab in 12 Fallen ein positives Resultat. Es zeigte sich, 
dass in alien zum Tode gekommenen Fallen die Bazillen sich wahrend 
des Lebens im Blut nachweisen liessen. Der friiheste Zeitpunkt, in 
dem uns bei den totlich endenden Fallen der Nachweis der Bazillen im 
lebenden Blut gelang, war 3 mal 24 Stunden vor dem Tode. In 
diesem friihen Zeitpunkte wurden in einem Fall 5 Kolonien auf 4 
Platten zu 2 ccm, in einem anderen 20 Kolonien auf 6 Platten zu 
2 ccm Blut gezuchtet. Bei der erst kiirzere Zeit vor dem Tode 
angelegten Blutkultur war die Zahl der Bazillen wesentlich grosser, 
wenige Stunden vor dem Tode waren die Platten mit Kolonien uber- 
sat. Im Leichenblut liess sich regelmassig der Milzbrandbazillus 
durch die Kultur nachweisen. 

Wenn wir vorerst die Falle unberiicksichtigt lassen, die mit einer 
Milzbrandbakteriiimie in unsere Behandlung kamen, deren positiver 
Blutbefund also schon von vornherein eine schlechte Prognose gab, 
so erzielte die konservative Behandlung sehr gute Resultate. Unter 


34 Fallen, deren Blutkultur bei der Aufnahme steril war, hatten wir 
nur einen Todesfall zu beklagen. Bei diesem, einem 28jahrigen 
Gerber, sass die Milzbrandpustel an der linken Halsseite ; es bestand 
ein sehr ausgebreitetes Oedem, doch war das Allgemeinbefinden kaum 
gestort, die Temperatur normal. Zwei Tage spater erfolgte, wie die 
Blutkultur ergab, der Einbruch der Bazillen in die Blutbahn unter 
Fieber bis zu 40.8 und 168 Pulsen. Zwei weitere Tage danach erlag 
der Patient seiner Milzbrandsepsis. In diesem Falle, in dem die not- 
wendige Ruhigstellung des Krankheitsherdes durch einen Verband 
wegen der Lokalisation am Hals nicht gut zu erreichen war und eine 
Ruhighaltung von dem Patienten wegen des fehlenden Krankheits- 
gefuhls nicht beobachtet wurde, versagte die konservative Therapie, 
In alien ubrigen Fallen, unter denen, wie aus der ausfuhrlichen 
Veroffentlichung des Naheren zu ersehen ist, sehr schwere Erkran- 
kungen mit weit ausgedehntem Oedem und schwer mitgenommenem 
Allgemeinbefinden waren, heilten die Kranken unter absoluter Ruhe 
und Analeptika, besonders Alkoholdarreichung. 

Ganz anders gestaltete sich die Prognose der Kranken, in deren 
Blut sich die Bazillen bei der Aufnahme nachweisen liessen. Wir 
mussten die Prognose bei ihnen nach unseren Erfahrungen absolut 
infaust stellen und erst in jungster Zeit haben sich uns auch fur diese 
Falle noch Heilungsmoglichkeiten ergeben in dem Salvarsan. 

let habe zuerst das Salvarsan am 20. V. 1911 bei einem 55 jahrigen 
Manne angewandt, bei dem aus 8 ccm. Blut 55 Kolonien geziichtet 
wurden und der einen so schweren allgemein septischen Eindruck 
machte, dass er von alien Beobachtern fur verloren angesehen wurde. 
Das Blut war an dem Tage nach der intravenosen Infusion von 0.6 
Salvarsan steril : die Temperatur fiel 2 Tage danach zur Norm ab und 
der Kranke genas. 

Dieser Fall schwerer Milzbrandbakteriamie ist bis jetzt der einzige 
durch Salvarsan geheilte geblieben. Wir hatten inzwischen nur noch 
bei zwei Fallen Gelegenheit, diese Therapie auzuwenden: in dem 
einen Falle war die in dem Blut vorhandene Bazillenmenge etwa 7 
mal so gross wie in dem geheilten Falle, also etwa 50 Kolonien in 1 
ccm., in dem anderen war das Blut schon uberschwemmt mit Bazillen 
und die Infusion wurde an dem moribunden Patienten gemacht, in 
beiden Fallen ohne Erfolg. Trotzdem halte ich mich fur berechtigt, 
diese eine Heilung einer schweren Milzbrandbakteriamie hier mitzu- 
teilen, weil es durch das Tierexperiment gelungen ist, die Wirksam- 
keit des Salvarsans bei der Milzbrandinfektion darzutun. 

Angeregt durch diesen Fall hat Herr Dr. Schuster in dem Stadt- 
krankenhaus Plauen i. V. Versuche an Kaninchen angestellt, die er 
mit einer 24stiindigen auf Agarschragrohrchen gewachsenen Rein- 
kultur eines hochvirulenten Milzbrandstammes infizierte. Es zeigte 
sich, dass ein Kaninchen durch eine gleichzeitig mit der subkutanen 


Milzbrandinfektion vorgenommenen intravenosen Salvarsaninfusion 
von 0.04 g. Kilo Tier gerettet wurde. Auch ein Tier, bei dem die 
Salvarsaninfusion 12 Stunden nach der subkutanen Milzbrandinfek- 
tion vorgenommen wurde, blieb am Leben und dauernd gesund. 
Auch bei einem intravenos mit Milzbrand infizierten Tier gelang es, 
durch eine fast gleichzeitig (etwa 3 Minuten spater) am anderen Ohr 
gemachten intravenosen Salvarsaninfusion das Tier zu retten, da- 
gegen starben die erst nach 12,4 oder 1 Stunde mit Salvansan 
behandelten Tiere, nachdem ihnen die Milzbrandkultur in die Vene 
eingespritzt worden war. Bei einer Wiederholung dieser Versuche 
mit der halben Salvarsanmenge, also 0.02 g pro Kilo Tier starben alle 
Tiere an Milzbrandsepsis. Das Ergebnis dieser Versuche, die mit 
sicherem Ausschluss von Versuchsfehlern und bei Aufstellung aller 
Kontrollen angestellt wurden, ist also, dass Salvarsan in einer Menge 
von 0.04 g pro Kilo Tier imstande ist, Kaninchen mit sonst sicher 
totlicher Milzbrandinfektion zu retten. 

Unabhangig hiervon wurden zu derselben Zeit von Laubenheimer 
Tierversuche in gleichem Sinne angestellt. Er verwendete Meer- 
schweinchen als Versuchstiere, die er subkutan infizierte und zwar mit 
0.1 g. Salvarsan pro Kilo Tier, also mit wesentlich hoherer Dosis wie 
Schuster. Die Resultate waren sehr ahnlich denen von Schuster : von 
den Tieren, die bis 20 Minuten nach der Infektion mit Salvarsan 
behandeit worden waren, starb nur eines an Milzbrand und auch 
dieses erst 22 Tage spater als das Kontrolltier. Aber auch noch 6 
Stunden nach der Infektion konnten bei einem Teil der Tiere durch 
die Salvarsaninjektion die in den Korper eingefuhrten Milzbrand- 
keime vollstandig abgetotet werden. Wenn die Salvarsanbehand- 
lung noch spater, 16-22 Stunden nach der Infektion einsetzte, so war 
der totliche Ausgang nicht mehr zu verhindern. 

Der Ausfall dieser Tierexperimente macht es wahrscheinlich, dass 
der giinstige Augang in meinem Fall schwerer Milzbrandbakteria- 
mie dem Salvarsan zu danken ist. Es ist ausserordentlich schwer, 
iiber die Wirkung des Salvansans auf den menschlichen Milzbrand ein 
sicheres Urteil zu gewinnen. Denn beweisend fur die Salvarsanwir- 
kung sind nur die Falle, in deren Blut die Bazillen nachgewiesen 
wurden, die anderen heilen, wie wir gesehen haben, auch bei Ruhig- 
stellung. Die Dauer der Anwesenheit der Bazillen im Blut ist aber 
nur kurz, nach unseren Erfahrunge etwa drei Tage vor dem Tode. 
Von dieser Zeit kann fur eine Heilwirkung des Salvarsans nur der 
Teil in Betracht kommen, in dem noch keine schrankenlose Vermeh- 
rung der Bazillen im Blut stattgefunden hat, indem also die in einem 
ccm. Blut gefundene BaziJlenmenge gering ist. Ist dagegen die mit 
1 ccm. Blut beschickte Kulturplatte mit Bazillen iibersiit, dann 
ist das Salvarsan unwirksam. Der Zeitraum im Verlauf einer Milz- 
brand^rkrankung, in dem die Salvarsananwendung einwandfrei als 


Heilwirkung sich darstellt, ist also sehr kurz, es ist das Anfangs- 
stadium der Bakteriamie. Um nicht missverstanden zu werden, 
mochte ich in aller Deutlichkeit aussprechen, dass ich bei dem Milz- 
brand, der immer die Gefahr einer Allgemeininfektion in sich 
schliesst und bei dem trotz fehlenden schweren Krankheitsgefiihls 
schon eine Bakteriamie bestehen kann, unbedingt die sofortige 
Anwendung des Salvarsans empfehle, sobald der Kranke sich in 
unsere Behandlung begibt. Ein Beweis fiir die Heilwirkung des 
Salvarsans ist durch diese Falle aber nicht erbracht, auch wenn wie 
es in beiden von Professor Bettmann (Heidelberg) mitgeteilten Fallen 
war, eine wesentliche Besserung nach der Injektion eintritt. Das 
subjektive Gefiihl des Beobachters und sein allgemeiner Eindruck 
sind zu unsichere Kriterien bei der Entscheidung dieser Frage. Es 
ware bedauerlich, wenn bei den Nachprufugen uber Salvarsanwirkung 
beim Milzbrand die Blutkultur nicht beriicksichtigt wiirde, wie es 
in England 1905 geschah, als auf die Anregung Legges hin das 
Milzbrandserum vielfach Anwendung fand und jeder, der 2 oder 3 
Falle behandelt hatte, uber seine Erfolge berichtete, ohne eine bak- 
terioiogische Kontrolle des Blutes vorgenommen zu haben. Es 
6ollte, wo es moglich ist, zugleich mit der Salvarsaninfusion eine 
Blutentnahme zur bakteriologischen Untersuchung gemacht werden, 
nur so ist es moglich, mit Sicherheit festzustellen, ob dem Salvarsan 
wirklich eine Heilwirkung bei dem Milzbrande des Menschen 

Report of a Joint Session of Sections I and V on Poliomyelitis, will 
be found in Volume /, Part II. 

Professor William H. Welch moved that an international com- 
mission be created, with Dr. A. Weber, of Berlin, as chairman, to 
standardize procedures for the study and differentiation of the 
typhoid-colon group, and to report at the next International Con- 
gress of Hygiene and Demography, and that this recommendation 
be transmitted to the Permanent International Commission for its 
approval. This motion was carried and was referred to the Per- 
manent International Commission. 

150 Section i. hygienic microbiology and parasitology. 
the belation of parasitic amebae to disease. 

By Chakles F. Craig, M. D., Captain, Medical Corps. United States Army, 

Washington, D. C. 


Within the past seven years it has been definitely proven that the 
parasitic amebae of man, or entamebae, are divided into several dis- 
tinct species, one of which is a harmless commensal ; that all cultural 
amebae which have been thoroughly studied are free-living species 
having nothing in common with the parasitic species; and that the 
latter have not been cultivated. 

These new developments in our knowledge of amebae necessitate a 
revision of some of our data connecting these organisms with disease 
in man, for all of the evidence gained by experiments on animals or 
man with cultural amebae must be discarded, as such evidence is of 
no value as showing the relation of parasitic amebae to disease in the 
human subject. In addition the results obtained experimentally in 
animals by feeding or injecting material containing entamebae must 
be revised in the light of the proven existence of a harmless and at 
least two pathogenic species. 

classification or amoebae. 

In considering the relation of entamebae to disease in man it is 
necessary to have a clear understanding of the classification of amebae 
in general. Loesch placed the ameba he found in man in the genus 
Amoeba, calling it Amoeba coli; in 1879, or four years after the dis- 
covery of Amoeba coli, Leidy established the genus Endamoeba for 
the parasitic ameba of the cockroach, described by Butschli under the 
name Amoeba blattae; in 1897 Casagrandi and Barbagallo, after a 
thorough study of the amebae occurring in the intestine of man, 
became convinced that they differed both in morphology and life- 
cycle from those occurring free in nature and, apparently unaware of 
Leidy's genus Endamoeba, established for the human parasites the 
genus Entamoeba. While eventually it may be determined that the 
spelling of Leidy must be retained, I prefer at the present time to 
accept the name Entamoeba for the parasitic amebae, as this term has 
been accepted and is used by almost every writer upon the subject. 

After the researches of Casagrandi and Barbagallo numerous 
attempts were made to separate the entamebae into distinct species, 
but it was not until 1903 that a clear description was given of at 
least two species of entameba occurring in man. During that year 
Schaudinn published his work upon parasitic amebae and differenti- 
ated two species — one a harmless parasite which he named Entamoeba 
coli; the other the cause of a form of dysentery, which he named 


Entamoeba histolytica. I was able to confirm Schaud inn's work in 
1905, and it has since been confirmed by many protozoologists in vari- 
ous parts of the world. Recently Prowazek found this species in 
dysentery cases in Samoa, and states that at no time in its cycle of 
development were cysts observed at all resembling those found in 
other parasitic species, but only the spore-like bodies described by 

A third species of entameba was described by Viereck in 1906. 
This parasite, which he named Entamoeba tetragena, occurred in 
cases of dysentery contracted in Africa, and his researches, as well 
as those of others, proved it to be a pathogenic species, and that it 
has a wide geographical distribution in the Tropics and subtropics, as 
well as in temperate climates. I have found this species in cases of 
dysentery contracted in the Philippines, Panama, and in New York, 
Illinois, Arkansas, and Wisconsin. At the present time some authori- 
ties believe that this species is identical with Entamoeba histolytica, 
but the point is far from proven, and until it can be shown that the 
process of reproduction by gemmation and spore formation, described 
by Schaudinn as characteristic of Entamoeba histolytica and con- 
firmed by myself in many cases of dysentery, occurs also in Enta- 
moeba tetragena, and that cases of tetragena infection occur which 
never present the characteristic four-nucleated cyst at any stage of 
the disease process, I am forced to consider the two species as dis- 
tinct, despite the fact that the nuclear structure of Entamoeba tetra- 
gena during certain stages of development resembles very closely 
that of Entamoeba histolytica. 

In addition to the three species mentioned^ several others have 
been described in man, as Entamoeba tropicalis, Lesage; Entamoeba 
minuta, Elmassian ; Entamoeba nipponica, Koidzumi ; Entamoeba 
williamsi, Prowazek; Entamoeba hartmanni, Prowazek; and Enta- 
moeba polecki, Prowazek. It is generally believed that most, if not 
all, of these species are founded upon insufficient data and that 
eventually they will be found to be identical with one or the other 
of the three species already mentioned. 

It may therefore be stated that at the present time most authorities 
recognize three distinct species of entamoeba as parasitic in man, i. e., 
Etamoeba coli, Entamoeba histolytica, and Entamoeba tetragena. 
These species have been carefully studied by numerous investigators 
in many parts of the world and are based upon marked differences in 
morphology and in the reproductive cycle. The nuclear structure of 
each species is distinctive, while Entamoeba coli forms cysts contain- 
ing eight daughter nuclei, this number being sometimes exceeded, 
Entamoeba tetragena cysts containing four daughter nuclei and 
Entamoeba histolytica cystlike bodies which are budded from the 


parent organism. In all these species the differences in the method 
of reproduction have been carefully studied and, in my opinion, con- 
stitute the most important basis of specific differentiation. 

The classification of the amebae that have been cultivated from 
the feces of dysenteric patients and from the pus of liver abscesses 
is in a most unsatisfactory condition. Several species and subspecies 
have been described by Whitmore, Walker, Williams, Werner, and 
others, but no agreement has been reached as to their exact specific 
status. For long regarded by Musgrave and Clegg, Walker, Lesage, 
and Noc as true parasitic species, identical with the species of enta- 
meba which have already been mentioned, these cultivated amebae 
have been shown to be free-living species of the Umax type by the 
more recent work of Hartmann : Werner, Whitmore, Walker, Liston 
and Martin, Wells, and the writer. All the cultural species that have 
been thoroughly studied contain a contractile vacuole, an organelle 
which is not present in any of the parasitic species of man, and they 
also differ greatly in their reproductive cycle. This subject will be 
referred to later in the discussion of the relation of these cultural 
species to disease. 


The following theories have been held regarding the relation of 
entamebae to disease in man: 1, that they are all harmless com- 
mensals ; 2, that they are secondary factors in the etiology of disease ; 

3, that all species of amebae are capable of causing dysentery; and 

4, that both pathogenic and nonpathogenic species are parasitic 
in man. 

Recent researches have shown that the latter theory, i. e., that 
pathogenic and nonpathogenic species of entamebae are parasitic in 
man is correct. It is still impossible to say whether some other 
factor is necessary before the pathogenic species can cause disease 
but the evidence all points to the contrary opinion. At the present 
time it is generally accepted that certain species of entamebae are 
capable of producing dysentery, but a few authorities still maintain 
that these parasites are only secondary invaders of the tissues and 
are not responsible for the lesions present. In support of this conten- 
tion they point to the fact that entamebae are found in many healthy in- 
dividuals and in patients suffering from diseases other than dysentery ; 
that dysentery occurs in epidemic and endemic form in regions where 
entamebae can not be demonstrated ; that many different agents when 
injected into the intestine are capable of producing lesions like those 
of amebic dysentery ; that direct infection of either animals or man 
with entamebae has never been proven; that the deductions based 
upon animal experiments are unsatisfactory; and that until we are 
able to cultivate the entamebae and to produce dysentery with pure 


cultures we are not justified in claiming that they are the cause of 
the disease. 

These objections, with the exception of the last mentioned, can all 
be answered by the results of work accomplished during the past 
few years. We know that the presence of entamebae in health and 
in disease other than dysentery is explained by the occurrence of a 
distinct species which is nonpathogenic and which is a parasite of 
man; that the occurrence of endemic and epidemic dysentery in 
regions where entamebae have not been demonstrated is due to the 
group of dysentery bacilli; that the lesions produced by the injection 
of either chemical or bacterial substances into the intestine are not 
identical with those produced by the entamebae; that direct infec- 
tion of animals with entamebae has been abundantly proven, and that 
such experiments are reliable when properly controlled. As regards 
the last objection, i. e., that until pure cultures are obtained the causa- 
tive relation of entamebae to disease can not be maintained, it may be 
stated that this is not a fair or valid objection, as there are other 
parasites well known to be the cause of specific infections which 
have not as yet been cultivated. 

In support of the etiological relation of certain species of entame- 
bae to dysentery we have the following facts: 1. The absolutely char- 
acteristic pathology of amebic dysentery and the constant presence of 
the pathogenic species of entamebae in the lesions and their absence 
from the lesions of other forms of dysentery ; 2, the constant presence 
of pathogenic entamebae in the tissues of the peculiar form of liver 
abscess which ofter complicates amebic dysentery; 3, the production 
of typical amebic dysentery in susceptible animals by feeding and 
inoculation experiments with material containing the pathogenic 
entamebae and the demonstration of the parasites in the lesions so 


It is not necessary at this time to discuss in detail the pathology of 
amebic infection. It is a self-evident fact to all who have had ex- 
perience with amebic dysentery at the autopsy table that the lesions 
of this disease are absolutely characteristic and are entirely distinct 
from those of the bacillary forms of the disease. I have had the op- 
portunity of studying hundreds of cases of both amebic and bacil- 
lary dysentery at autopsy, and can state that one may easily dis- 
tinguish the lesions produced by the entamebae from those due to 
other causes. 

If sections are made through the lesions in the intestine, entamebae 
may be demonstrated in every portion of the involved region. They 
are frequently numerous in the mucous, submucous, and muscular 
coats of the intestine, where they may be demonstrated in the 
glandular tissue, in the intermuscular septa, and in the lymphatics 
and blood vessels. Of course, in the intestine, it can not be denied 


that a portion of the pathological picture may be due to bacteria 
which have gained entrance to the tissues along with the entamebae, 
but the fact remains that the latter organisms are always associated 
with a characteristic ulcerative lesion never produced by bacteria 

I believe that if we had no other evidence than the peculiar lesions 
of this form of dysentery with which are always associated the patho- 
genic species of entamebae we would be justified in considering the 
latter as the cause of the disease. 

It is well known that a peculiar form of liver abscess frequently 
complicates amebic dysentery. The pathology of this condition is 
characteristic and in the contents of such abscesses entamebae can 
always be demonstrated and if sections are made of the abscess wall 
these organisms are found within the tissues. Frequently the ab- 
scess contents are sterile save for the entamebae, while the most care- 
ful staining of the tissues fails to reveal any other etiological factor. 

The experimental production of ,dysentery in susceptible animals 
with entamebae dates back practically to the discovery of these para- 
sites. Loesch produced the disease in a dog by the rectal injection of 
fecal material containing entamebae and his results were confirmed 
upon cats by Hlava, Kovacs, Kartulis, Zancoral, Strong, and Mus- 
grave, and many others. Huber produced dysentery in dogs by feed- 
ing them feces containing entamebae and Kruse and Pasqualle 
produced the disease in cats with the pus from an amebic liver 
abscess. The work of Harris, which has been largely overlooked by 
writers dealing with this question, was of great interest and im- 
portance. He endeavored to produce dysentery in dogs by the rectal 
injection of various bacteria and fecal material from dysentery cases. 
Among the bacteria injected were the typhoid bacillus, colon bacilli, 
anthrax bacilli, pyogenic cocci, the dysentery bacillus of Shiga and 
mixed cultures of bacteria from dysentery patients. His experiments 
; were most carefully controlled and in not a single instance did the 
animals show any evidence of disease following the injection of the 
bacteria. On the other hand the injection of fresh feces containing 
entamebae in the rectum of puppies was followed in every case by a 
typical dysentery resulting in the death of the animal experimented 
upon. In two of the animals amebic abscess of the liver developed 
and entamebae were recovered from the abscess pus. In all of the 
animals, four in number, the lesions present in the intestine were 
typical of those found in amebic dysentery in man. The period of 
incubation varied from three to six days. Sections of the intestine 
of the infected animals exhibited the microscopic pathology of amebic 
dysentery and the entamebae were demonstrated in the tissues. 

All the experimental work cited, while conclusive as to the produc- 
tion of dysentery in susceptible animals with material containing 


entamebae, is inconclusive as regards the exact species used in the 
experiments, as these researches were made before Schaudinn's work 
in species differentiation. Since his observations, however, numerous 
investigators have proven that Entamoebas coli is not a pathogenic 
organism and that Entamoebas histolytica and Entamoebas tetragena 
are the species most frequently concerned in the etiology of amebic 


Entamoebae coli is a species frequently observed in the feces in 
both health and disease. Although it is probably world-wide in 
its geographical distribution the percentage of infection varies 
greatly in different localties, being highest in tropical countries and 
lowest in cold climates. 

Schaudinn found it present in 50 per cent of healthy individuals 
in West Prussia, in 20 per cent in Berlin, and 66 per cent of healthy 
people examined on the shores of the Adriatic Sea; Vedder, in 50 
per cent of healthy American soldiers, and 72 per cent of Filipino 
scouts in the Philippines; Sistrunk, in 11 of 145 patients suffering 
from diseases other than dysentery in the Mayo Hospital at Koches- 
ter, Minn, the patients coming from different parts of the United 
States ; and Ashburn and the writer in 71 per cent of healthy Ameri- 
can soldiers in Manila. In 1905 I examined over 200 American 
soldiers in San Francisco, who were recruited from different parts of 
the United States, and found that 65 per cent of them showed 
Entamoeba coli in the stools after a saline cathartic. This species 
has lately been demonstrated by Stiles in North Carolina, by McCar- 
rison in India, and its occurrence in the Philippines confirmed by 
Whitmore and Walker. It has also been found upon the Isthmus 
of Panama by Darling and James, in South America by Elmassian, 
and in Samoa by V. Prowazek. 

That this organism is not pathogenic has been proven by many in- 
vestigators. Its common occurrence in healthy individuals, in whom 
it has been observed for months and even years without producing 
symptoms of diarrhea or dysentery, and the negative result of animal 
experiments by numerous investigators prove that this species is a 
harmless commensal of the human intestine. Negative results were 
obtained by Kartulis, Kruse and Pasquale, Celli and Fiocca, Strong 
and Musgrave, Kovacs, and Jiirgens by injecting material containing 
entamebae parasitic in healthy individuals, and Schaudinn showed 
that this entameba, which he called Entamoeba coli, is capable of 
living in the intestine, but that it never produces symptoms of 
diarrhoea or dysentery either in animals or man. 

I have made many attempts to produce dysentery in kittens with 
Entamoeba coli, both by injecting fecal material containing them into 


the rectum and by feeding material containing both the encrysted 
and vegetative forms, but have never been able to produce the least 
symptom of dysentery, although 50 per cent of the kittens given 
rectal injections of feces containing Entamoeba histolytica and 65 per 
cent of kittens fed with milk infected with material containing the 
same species developed severe dysentery. 

In a recent personal communication Dr. Creighton Wellmann has 
furnished me with some data regarding experiments with Entameba 
coli. He infected five kittens by injecting 4 to 5 cubic centimeters of 
feces containing encysted Entamoeba coli into the rectum. All the 
animals remained perfectly well and were killed about one month 
after the injection. In none of them were any evidences of dysenteric 
lesions found at autopsy. 

From the evidence which has accumulated it may be positively 
stated that Entamoeba coli is not a pathogenic parasite and that it has 
been found in a considerable proportion of healthy individuals in 
every region where it has been carefully searched for. This parasite 
is chiefly of importance because of the liability of confusing it with 
the pathogenic entamebae, and there can be no question that hundreds 
of cases of so-called amebic dysentery have really been diarrhoeas due 
to other causes, but so diagnosed because of the finding of Entamoeba 
coli in the stools. 


I have already mentioned the numerous instances of the produc- 
tion of dysentery with material containing entamebae, but Schaudinn 
was the first to demonstrate the actual species concerned in many of 
these experiments. This species he named Entamoeba histolytica and 
he conclusively proved that it is the cause of a form of dysentery and 
that the so-called spores of this parasite are infective. He thus de- 
scribes his experiments, which prove this point : 

From this case I took a small quantity of feces, divided it into three parts, 
dried each in the air, and mixed with it sufficient water for about 20 crush 
preparations under cover glasses. These preparations were carefully examined, 
the examination being conducted upon a mechanical stage and requiring many 
hours. No forms resembling the cysts of Entamoeba coli were found, but the 
small spores of Entamoeba histolytica were noticed in large numbers, but no 
vegetative organisms could be demonstrated. The cover glasses were then 
removed, the feces washed with distilled water, and ten such preparations were 
mixed with enough distilled water to form 1 cubic centimeter of the mixture. 
The feces of the animal to be experimented upon — a healthy, strong young cat — 
was carefully examined for amebae and none could be demonstrated. To this 
cat I gave the 1 cubic centimeter preparation mentioned above, mixing it with 
milk. On the evening of the third day the cat passed bloody mucoid feces and 
an examination showed the presence of great numbers of typical Entamoeba 
histolytica. In the afternoon of the fourth day the cat perished. Dissection 


showed typical ulcerous dysentery of the large intestine and immigration of 
the amebae into the epithelium could be easily established. 

I will mention yet another experiment which goes to prove that the perma- 
nent spores by themselves are capable of producing a new infection. The feces 
of the cats developing dysentery contained only vegetative stages of the amebae, 
no spores being found. When large quantities of the feces were given to a cat 
it remained well and for four weeks showed no amebae in its feces. It was then 
fed with the remnant of the dried feces used in the first experiment, which con- 
tained multitudes of the spores, and after six days the amebae began to appear 
in the feces. Being older and larger than the other cat, it proved more resist- 
ant to the infection and did not die until two weeks later. The autopsy showed 
the lesions of typical amebic dysentery. 

Schaudinn's worl£ served to explain the negative results of some 
observers with Entamoeba histolytica. During the active stage of 
dysentery only the vegetative forms of this species occur in the feces, 
and as these forms are not infective the experiments in which only 
material containing these forms are used will give negative results. 
However, if the feces from cases which are recovering from dysen- 
tery are used for experimental purposes a large proportion of sus- 
ceptible animals will develop the disease, as at this stage of the 
disease the infective sporelike cysts are present. 

In 1905 I was able to confirm Schaudinn's work regarding the 
pathogenic nature of Entamoeba histolytica. Half-grown kittens 
were used in my experiments, and 50 per cent of those given rectal 
injections developed the disease, while 66 per cent of the feeding 
experiments were successful. It will be noted that the latter method 
gave the best results, as 8 of the 12 kittens experimented with de- 
veloped dysentery, Entamoeba histolytica being found in the feces 
and in sections of the diseased intestine. One of the animals de- 
veloped an amebic abscess of the liver, and this species of entameba 
was found in the abscess contents as well as in sections of the abscess 
wall. The period of incubation varied from 6 to 14 days, being 
slightly shorter in the feeding experiments than after rectal injection. 

All the kittens experimented upon were carefully examined for 
amebae prior to the experiments so as to rule out a previous infec- 
tion. Both pure and mixed cultures of all bacteria that could be 
cultivated from the feces were fed and injected in order to control 
the tests, and in none of the kittens so treated did the symptoms of 
diarrhoea or dysentery develop, and at autopsy no lesions were found 
in the intestine. 

In dysentery produced by the rectal injection of the infected ma- 
terial the lesions were usually localized in the rectum and were not so 
severe, as a rule, as when the infection was acquired through the 
mouth. The lesions produced were typical of those occurring in 
amebic dysentery in man and varied in extent and severity with the 
length of time the infection lasted. The symptoms consisted of 


diarrhoea with the passage of blood-stained mucous stools, containing 
multitudes of motile Entamoeba histolytica; rapid emaciation with 
loss of appetite and strength ; and finally death from exhaustion. In 
a few instances attacks of severe diarrhoea were followed by a period 
of constipation and the disease became chronic in nature. The 
longest period of incubation was 14 days in a kitten injected per 
rectum and the shortest period 6 days in an infection by the mouth. 

The following protocols of autopsies will illustrate the lesions pro- 
duced in kittens by Entamoeba histolytica. 

Kitten No. 1. — This kitten was injected per rectum on October 19 
and killed upon November 21, the first evidence ef infection having 
appeared about October 30. 

Kitten No. 2. — Body that of a half-grown kitten very greatly 
emaciated. The abdomen is greatly distended with gas. The mucous 
membrane of the anus appears swollen, and a considerable amount 
of blood-stained mucus is adherent to it. The subcutaneous fat has 
almost entirely disappeared and the muscles appeared dry and 
atrophied. The pleural cavities are free from fluid and the lungs 
appear normal. The heart is greatly congested and contains red clots 
in all the chambers. The liver is hypertrophied, deeply congested, 
and marked albuminoid degeneration is present but there is no trace 
of abscess formation. The kidneys are congested and upon section 
present the usual lesions of an acute parenchymatous nephritis. The 
omentum contains a small amount of fat and is not inflamed. The 
bladder is filled with urine. 

The intestines are greatly dilated with gas and fluid. Upon exter- 
nal examination the large intestine appears swollen, is grayish in 
color, with small, darker colored areas scattered along it. Upon 
opening the large intestine the mucous membrane of the rectum is 
found considerably swollen and inflamed, but no ulcerations are 
present. Above the rectum for a distance of about 10 centimeters the 
mucous membrane is very much swollen and edematous, bright red in 
color, and between the folds a considerable amount of pus can be 
seen. For a distance of about 4 centimeters from the upper end of 
the large intestine, the mucous membrane is inflamed, being red, 
swollen, and edematous. In this area there are numerous ulcerations 
covered in with bloody mucus; they are of small size, somewhat 
irregular in shape, and extend in most instances to the submucosa, 
although there are a few which extend to the muscular coat of the 
intestine; the edges are undermined and many of the ulcers are cov-. 
ered with necrotic tissue, brownish yellow in color, which has to be 
removed in order to expose them. A few of the ulcers communicate 
beneath the mucous membrane. The small intestine shows a rather 
severe acute enteritis and the stomach an acute gastritis. 


Kitten No. 3. — This kitten was fed once with feces containing 
Entamoeba histolytica, and seven days later developed diarrhoea, the 
feces containing blood and mucus : as well as numerous motile amebae. 
At the end of two weeks it died, having presented severe symptoms of 
amebic dysentery during this time. 

Autopsy: Body that of a half-grown kitten, very greatly emaci- 
ated. Subcutaneous fat entirely absent, and muscles dry and much 
atrophied. The abdominal cavity is free from fluid and the intes- 
tines appear normal externally. The pleural cavities are free from 
fluid and the heart and lungs appear normal. The liver is brownish 
red in color externally with irregular yellow mottlings. There is a 
small abscess present at the dome of the right lobe, measuring 0.25 
centimeter in diameter, showing very distinctly through the capsule 
of the organ. Upon section of the liver the cut surface appears 
greatly congested, the lobules are distinct, and no abscesses are found 
other than the one mentioned. The gall bladder appears normal. 
The kidneys appear enlarged and congested and upon section show 
an acute congestion, with some thickening of the cortex. Externally 
the large intestine appeared slightly, if at all, congested, although the 
walls were markedly thickened. Upon opening the large intestine it 
was found filled with fecal material mixed with a large amount of 
pus and blood-stained mucus. About 1 centimeter from the anus, 
which was blood stained and covered with mucus, there was an area 
measuring 4 centimeters in length presenting the typical lesions of 
amebic dysentery as they are observed in man. The entire mucous 
membrane was swollen, congested, and edematous. Numerous nodu- 
lar areas projected into the lumen of the intestine, which, when 
incised, were found filled with a glairy material containing hundreds 
of Entamoeba histolytica. There were also numerous ulcerations, more 
or less irregular in shape, with thickened and undermined edges; 
many were covered in with necrotic tissue, which, upon being re- 
moved, showed that the floor of the ulcer was formed by the muscular 
coat of the intestine. Many of these ulcers communicated with one 
another beneath the mucous membrane and most of them had pene- 
trated to the muscular coat. The remainder of the large intestines 
presented numerous ulcerations typical of those seen in the intestine 
of patients who have died of amebic dysentery. The lesions were 
most marked just below the ileo-cecal valve, where large areas of the 
mucous membrane had been destroyed, the muscular coat of the intes- 
tine being exposed. 

Kitten No. 5. — This kitten was fed with milk containing Entamoeba 
histolytica several times before dysentery developed. The period 
of incubation was eight days from the date of the last feeding, but 
from that time until it was killed, three weeks afterwards, the animal 
presented the symptoms of amebic dysentery, there being gradual loss 


of appetite, emaciation, and a diarrheal discharge containing blood 
and mucus with numerous motile Entamoeba histolytica. 

Autopsy: Body that of a half-grown kitten, much emaciated. 
Subcutaneous fat entirely absent and muscles much atrophied. The 
pleural cavities were free from fluid and the lungs and heart ap- 
peared normal save for congestion. Upon opening the abdominal 
cavity the small intestine appeared congested externally. The liver 
is hypertrophied and greatly congested. The kidneys are congested 
and enlarged and upon section showed the lesions of an acute paren- 
chymatous nephritis. The large intestine was dark gray in color 
externally and was considerably thickened, especially toward the 
rectum. Upon opening the intestine it was found to contain much 
fecal material, mixed with blood, mucus, and pus. Commencing at 
the rectum and extending for about half the length of the large intes- 
tine, the mucous membrane was greatly swollen, bright red in color, 
and contained numerous ulcers. The majority of the ulcers were 
spherical in shape, the edges were undermined and greatly thickened, 
and many were covered in with necrotic tissue. Upon removing this 
necrotic material the base of the ulcer is found to be formed by the 
muscular coat of the intestine. The ulcers present were typical of 
the amebic ulcerations seen in the intestine of man in every respect. 
The remainder of the large intestine was black in color and gan- 
grenous, the mucous membrane having been almost entirely destroyed, 
exposing the muscular coat throughout this portion of the intestine. 
About 4 centimeters below the ileocecal valve there was a small 
perforation measuring about one-sixth centimeter in diameter. 

The following interesting cases of experimental infection with 
Entamoeba histolytica have been furnished me by Dr. Creighton 
Wellman. His data cover five kittens, of which four developed dys- 
entery and one remained free from the disease. 

Kitten No. 18. — On August 20, 1910, 4 to 5 cubic centimeters of 
feces containing the cysts of Entamoeba histolytica were injected per 
rectum. The kitten remained apparently healthly until September 
1, when entamebae were found in the feces. From this time on the 
animal grew steadily worse and the number of entamebae increased. 
The animal was killed September 21, and the following conditions 
were found at autopsy: Great emaciation, heart and lungs normal, 
liver enlarged but with no abscesses. Kidney showed the signs of 
nephritis. The mucous membrane of the large intestine was inflamed 
and edematous, and there were numerous small ulcerations, scrapings 
from which showed many entamebae. The small intestine and the 
stomach appeared to be somewhat injected. Dr. Wellman stated: 
" I should call the condition found a typical amebic dysentery." 

Kitten No. 19. — The same technique was employed in infecting 
(his kitten. This animal developed dysentery and Entamoeba histoly- 


tica was found in the feces. The autopsy record of this animal is 
not given. 

Kitten No. 20. — This kitten was fed with 4 to 5 cubic centimeters 
of the same feces used in infecting the kittens already mentioned. 
After 8 days entamebae were found in the stools and the animal died 
on the fifteenth day after infection. The following conditions were 
found at autopsy: The kitten was much emaciated, heart and lungs 
normal, liver swollen and congested but showing no abscesses. The 
kidneys showed the evidences of nephritis. The mucous membrance 
of the entire large intestine showed typical amebic ulcerations, many 
of them burrowing in character. The scrapings from the ulcers 
showed numerous entamebae. The entire intestine appeared 

Kitten No. 23. — This animal was fed with the same feces, and enta- 
mebae appeared in the stools on the ninth day after feeding. It was 
killed on the eighteenth day after infection and the same condition 
found as in kitten No. 20, but the lesions were not quite so severe. 

Kitten No. 2Jf. — This animal was fed with the same feces, but with 
negative results. No entamebae appeared in the feces and no lesions 
were found in the intestine when the kitten was killed on the twenty- 
eighth day after feeding. This animal was considerably older than 
the others experimented with, and I have found that for successful 
results young kittens must be used, as full-grown cats are much more 
resistant to amebic infection. 

Wellman states in his letter that he considers the lesions produced 
experimentally in these kittens as identical with those of amebic 
dysentery in man. More recently Werner, working at the Sailor's 
Hospital, in Hamburg, has produced dysentery in cats with Enta- 
moeba histolytica. 

He experimented with two strains of Entamoeba histolytica, only 
one of which he found infective. He was able to produce dysentery 
in cats with this strain, but found that after six passages the organ- 
ism lost its virulence. The incubation period varied from 4 to 13 
days, the average being 9 days. Of six cats infected with this species 
four died, the duration of the disease varying from 7 to 24 days, the 
average being 15 days. The animals were infected per rectum. 
Werner states that the lesions were typical of amebic dysentery and 
were always confined to the colon, especially the lower portion. 
Guinea pigs and rats were found to be resistant to infection with this 

From the evidence which has been submitted I believe it is impos- 
sible to conclude otherwise than that Entamoeba histolytica is the 
cause of a form of amebic dysentery. The character of the lesions 
present in this condition, the constant association of this species with 
66692— vol 2, pt 1—13 11 


the lesions, and the production of similar lesions in susceptible animals 
with material containing Entamoeba histolytica I consider conclusive 
proof that this parasite is a cause of amebic dysentery in man. 


The experiments of Viereck, Hartmann, and Werner prove that 
this species produces a form of dj^sentery, although Hartmann be- 
lieves that it is not as pathogenic to cats as Entamoeba histolytica. 
The incubation period in his experiments varied from 8 to 10 days 
and the infection lasted from 3 weeks to a month. He states that at 
autopsy the cats presented the typical lesions of amebic dysentery as 
observed in man and that Entamoeba tetragena was found in the 

Werner experimented with 5 strains of Entamoeba tetragena, only 
3 of which were found to be pathogenic. One of these was still in- 
fective after 5, one after 3, and one after 1 passage through cats, 
but they all lost their virulence after repeated passage. The incu- 
bation period in his animals varied from 5 to 12 days, and the 
disease lasted from 3 to 25 days, the average being 17 days. He 
states that he did not find any marked differences between the lesions 
produced by tetragena and histolytica and that he does not believe 
that the evidence supports the idea that one is less pathogenic than 
the other. 

Werner describes an interesting experimental case in which a cat 
infected per rectum with a strain of tetragena developed dysentery 
after 5 days incubation, the stools containing many entamebae. At 
the end of 12 days the animal died and at autopsy typical amebic 
ulcers were found in the lower portion of the colon, while the right 
lobe of the liver showed an abscess the size of a hazel nut upon the 
anterior surface. The pus from the abscess contained entamebae 
of the tetragena type. 

Franchini reports the production of dysentery in a monkey by 
rectal injections of fecal material containing Entamoeba tetragena. 
The monkey experimented upon had been under observation in the 
laboratory for over a year, was perfectly healthy, and repeated 
examinations of the feces before the experiment showed them to be 
free from entamebae. After the rectal injections of material con- 
taining Entamoeba tetragena the animal developed an intense dysen- 
tery, the stools containing blood, mucous, and multitudes of en- 
tamebae identical in morphology with those injected. The animal 
died from the infection and at autopsy ulcers were found in the 
large intestine and Entamoeba tetragena was demonstrated in sections 
of the diseased tissues. 

In a personal communication Dr. H. B. Fantham states that he 
was successful in producing dysentery in one of two kittens fed upon 


feces containing Entamoeba tetragena from an infection contracted 
in Algeria. The kitten died in 3 weeks, and ulcerations were found 
in the intestine which contained Entamoeba tetragena. His experi- 
ments in kittens with rectal injections of material containing this 
parasite were all negative. 

I have had no personal experience with the experimental produc- 
tion of dysentery in animals with this species, but I consider the 
evidence sufficient to prove that it is capable of causing the disease 
in susceptible animals and that it is a very frequent cause of dysen- 
tery in man. I have found Entamoeba tetragena in patients suffering 
from dysentery contracted in the Philippine Islands, Panama, and 
several of the United States. 


As several authorities have reported instances of the production 
of dysentery in animals with cultures of amebae it is necessary to 
consider briefly this phase of our subject. I have already stated 
that it has been proven by numerous investigators that all cultural 
amebae, that have been thoroughly studied, belong to the genus 
Amoeba and differ in morphology and life cycle from the parasitic 
species belonging to the genus Entamoeba, and that there is no suffi- 
cient proof that any of the latter species have been cultivated. 

Prior to the work of Musgrave and Clegg several authorities 
claimed to have produced dysentery in cats with cultures of amebae, 
while others were unsuccessful in thus producing the disease. It is 
unnecessary to consider here the conflicting results obtained by such 
investigators as Kartulis, Vivaldi, Cassagrandi and Barbagallo, and 
Zaubitzer along this line, but the work of Musgrave and Clegg 
deserves special consideration. These authors were successful in 
cultivating numerous strains of amebae in symbiosis with bacteria 
from the feces of dysenteric patients and from liver abscess pus. 
They refused to accept the classification of Schaudinn and considered 
that all amebae might, under certain circumstances, become patho- 
genic: They were successful in producing ulcerations of the 
intestine and liver abscess in monkeys with mixed cultures of their 
amebae and various bacteria, and in one instance they claim to have 
produced amebic dysentery in man with a pure mixed culture of 
amebae isolated from the stools of a dysenteric patient. 

In the light of -our present knowledge these experiments of Mus- 
grave and Clegg have no value as showing the relation of entamebae 
to disease. The work of Hartmann, Werner, Whitmore, Walker, 
and the writer has proven conclusively that the amebae cultivated 
by these authors are not entamebae but free-living amebae, and the 
species with which Musgrave and Clegg claim to have produced 


dysentery in man is a typical free-living ameba of the Umax type. 
The occurrence of dysentery after the administration of this culture 
can be explained in many ways: The culture may have become in- 
fected with the cysts of tetragena or histolytica, or the man have 
become naturally infected or have been infected at the time of the 
experiment, for in a region such as Manila natural infections would 
be very difficult to guard against. As regards the lesions produced 
in monkeys with cultures of amebae it should be remembered that 
these animals suffer naturally from amebic infection, and there is 
no evidence in the authors' papers that repeated examinations of 
the animals' stools were made for a sufficient period of time before 
the experiments to prove their freedom from entamebae. 

The occurrence of dysentery in monkeys after feeding or injecting 
cultural amebae is probably explained, in the vast majority of 
instances, by the fact that at least two species of entameba are 
parasitic in monkeys, as shown by Castellani and v. Prowazek, and 
that these species are capable of producing dysentery in these ani- 
mals. Greig and Wells have also shown that in India natural 
amebic infection in monkeys is very common; thus every one of 53 
monkeys with which they desired to experiment showed amebae in 
the feces which resembled those found in man. These organisms 
only appeared at irregular intervals, so that repeated examinations 
of the feces were necessary in order to demonstrate them. Some of 
the animals presented symptoms of dysentery while under observa- 
tion, while others appeared perfectly healthy. I do not know the 
percentage of monkeys infected with entamebae in the Philippines, 
but I personally observed three naturally acquired amebic infec- 
tions in these animals in Manila, and I have no doubt that careful 
examinations, covering a sufficient period of time, would demonstrate 
that a considerable percentage of monkeys in these islands harbor 
entamebae which could easily be confused with those parasitic in 

In many of their experiments (Musgrave and Cleggs) the amebae 
were grown in symbosis with the typhoid bacillus, and this mixed 
culture was injected directly into the liver subcutaneous tissue, or 
the abdominal cavity of the animals used, and was followed by the 
appearance of abscesses containing both amebae and bacteria. It 
is well known that the typhoid bacillus is capable of producing 
abscesses when thus injected, and I have observed the formation of 
abscess of the liver after the injection of pure cultures of this organ- 
ism into the organ, so that deductions based upon such experiments 
are valueless as proving the pathogenicity of any ameba. Even 
though lesions were produced in animals with these cultures of 
amebae they would bear no relation to the disease as it occurs in 
man, because the cultivated amebae are entirely distinct from the true 


parasitic amebae which cause dysentery in man. Personally I be- 
lieve that some of the lesions described by Musgrave and Clegg were 
produced by the mixed cultures of amebae and bacteria, with which 
they worked, but I can not admit that the cultural amebae are identi- 
cal with the parasitic species, or that their experiments are of any 
value as showing the relation of entamebae to disease. 

The claim of Musgrave and Clegg that the differences in structure 
and life cycle of the cultural amebae are due to artificial surround- 
ings can not be accepted. Walker, in discussing this argument, very 
justly says: " That while slight modifications might occur under such 
conditions, it is very improbable that cultivation could cause a com- 
plete reorganization of the structure of the nucleus, develop de novo 
such a constant organelle as a contractile vacuole, or profoundly 
modify the life cycle of the organisms. Moreover, that the supposed 
modification should invariably take the form of a change from the 
characters of the genus Entamoeba to those of the genus Ameba is, to 
say the least, improbable." 

It is not difficult to explain the ocurrence of free-living amebae 
in cultures made from feces, liver abscess pus, or from the intestine 
at autopsy, if one remembers that the cysts of these species are pres- 
ent in the atmosphere, and may thus easily contaminate the cultural 
material. The recent observations of Liston and Wells prove that 
it is possible to secure cultures of free-living species of amebae upon 
media exposed to the air, the organisms in such cultures agreeing in 
morphology with those obtained in cultures from the feces and 
intestine. Though it is possible for the free-living species to pass 
through the intestinal canal of animals in an encysted state and 
afterwards develop in cultures, it should be remembered that unless 
the most careful cultural technic is used such amebae may contaminate 
the cultures from the atmosphere, and it is probable that this is the 
manner in which many cultures have been obtained, especially in 
regions where the free-living species are found abundantly. How- 
ever, it is very difficult to understand how anyone possessing accu- 
rate knowledge of the morphology and life history of amebae could 
mistake these cultural species for any of the entamebae of man. 


The following conclusions appear to be justified as regards the 
relation of entamebae to disease. 

1. Entamoeba coli is a harmless commensal in the human intestine. 

2. Entamoeba histolytica and Entamoeba tetragena are pathogenic 
species capable of producing in man the disease known as amebic 

3. Entamoeba coli, Entamoeba histolytica, and Entamoeba tetra- 
gena are strictly parasitic species and have not been cultivated. 


4. There is not sufficient evidence at present to prove that any of 
the ameba that have been cultivated are pathogenic to man. All 
cultivated species belong to the genus Amoeba and differ greatly in 
morphology and life cycle from the parasitic ameba, which belong to 
the genus Entamoeba. 


The references are arranged alphabetically and only papers which have been 
consulted in preparing this paper are included in the list : 
Ashburn, P. M., and Craig, C. F., Entamoeba coli, etc. The Military Surgeon. 

1907. I. p. 21. - 

Casagrandi, O., and Barbagallo, P., Recersche Biolog. e. Clinishe dell "Amoeba 
coli " Boll. Accad. Groinea. sc. nat. Catania. 1895. xli. p. 7. 

Idem. Entamoeba hominis a amoeba coli (Loesch). Anali d'Igiene speri- 
mentale, 1897. V. p. 103. 

Castellani, A., Note on a Liver Abscess of Amoebic Origin in a Monkey. Para- 
sitology. 1908, I, p. 101. 

Celli, A., and Fiocca, R., Ueber die Etiologie der Dysenterie. Centralbl. f. Bakt, 
etc., 1895, I, xvii, p. 309. 

Craig, Chas. F., Observations upon Amoebae Infecting the Intestine, etc., Am. 
Med. Phila. 1905, IX, pp. 854, 897, 937. 

Idem. Studies upon Amoebae in the Intestine of Man. Jour. Infect. Diseases. 

1908. 5, p. 324. 

Idem. Entamoeba tetragena as a Cause of Dysentery in the Philippine Islands. 

Arch. Inter. Med. 1911, VII, p. 362. 
Idem. The Parasitic Amoebae of Man. 1911. Philadelphia. 
Idem. Observations upon the Morphology of Parasitic and Cultural Amoebae. 

Jour. Med. Research, 1912, XXVI, p. 1. 
Idem. The Parasitic Amoebae of Man and their Relation to Disease. New 

Orleans Med. and Surgical Jour. 1912. XXX. p. 1. 
Darling, S. T., Rep. Dept. Sanit. Isthmian Canal Commis., 1912. March, p. 42. 
Elmassian, Entamoeba minuta, etc., Centralbl. f. Bakt., etc., 1909, Abt. Orig. 

52, p. 335. 
Fantham, H. B., Personal Communication. 

Greig, E. D., and Wells, R. T., Dysentery and Liver Abscess in Bombay. Scien- 
tific Mem. Sanit. Dept's. Gov't. India. N. S. 47. 1911. 
Harris, H. F., Hatfield Prize Essay. Philadelphia, 1901. 
Franchini, G., Experimentelle Tropendysenterie, die Entamoeba beim Affen. 

Centralbl. f. Bakt., etc. 1912. I. Abt. Orig. 61, 7, p. 590. 
Hartmann, M., Eine neue Dysentery amoeba. Beiheft. z Arch. f. Schiffs-u 

Tropenhyg., 1908, V, p. 117. 
Idem. Untersuchungen u. parasitischen amoben. I, Entamoeba histolytica, 

Schaudinn. Arch. f. Protistenk. 1909. XVIII, p. 207. 
Idem. Die Dysenterie-Amoben. Handbuch der Pathogenen Protozoen. v. Prowa- 

zek. Leipzig. 1911. I, p. 50. 
Idem. Untersuchungen u. parasitische Amoben. II. Entamoeba tetragena, 

Viereck. Arch. f. Protistenk. 1912, XXIV, p. 163. 
Hlnva, Ueber die Dysenterie. Centralbl. f. Bakt., etc., 1887. Abt X, p. 537. 
Huber. Deutsche. Med. Wochenschr., 1903, XXIX, p. 267. 
James, W. M., Personal Communication. 
Jurgens, Zur Kenntnlse der Darmamoeben und der Amoemen-enteritis. Veroff. 

a. d. Oeb. Milit-Sanitatswes. Berlin, 1912. 20, p. 110. 


Kartulis. Zur Aetiologie der Dysenterie in Aegypten. Virch. Archiv. f. path. 

Anat. 1886. ex, p. 521. 
Koidzurui, M., On a New Parasitic Amoeba, Entamoeba nipponica. Centralbl. f. 

Bakt., etc., 1909. I, Orig. li. p. 650. 
Kovacs, F., Amoeben Dysenterie. Zeitschr. f. Heilkde. 1892. xiii, p. 509. 
Kruse, W., and Pasquale, A., Studium des Dysenterie und Leberabscesse. 

Deutsche, med. Wochenschr. 1893, 15, I. p. 354 ; 16, p. 368. 
Lesage. Note sur l'Entamibe de la dysenterie amibiene, etc., Bull. d. l'Soc. d. 

Path. Exotique. 1908, I. p. 104. 
Llston, W. G., and Martin, C. A., A Note on the Early Stages of Nuclear Division 

of the Large Amoeba from Liver Abscesses. Quar. Jour. Microscop. Science. 

N. S. 1911. 226, p. 279. 
Loesch, F., Massenk. Entw. v. Amoeben in Dickdarm. Virch. Arch. f. Path. Anat. 

1875, lxv, p. 196. 
Musgrave, W. E., and Clegg, M. T., Amebas : Their Cultivation and Etiological 

Significance. Bureau of Govt., Lab. Bull., Biological Lab., 1904, 18, Manila, 

P. I. 
Idem. The Cultivation and Pathogenesis of Amoebae. Philippine Jour., 

Science. 1906, I, p. 909. 
Noc, F., Sur la Dysenterie Amibiene en Cochinchine. Ann. Inst. Pasteur. 1900, 

XXIII, p. 177. 
Prowazek, S, v. (and Hartmann, M.,) Arch. f. Protistenk., 1909, xviii, p. 312. 
Prowazek, S, v., Entamoeba buccalis. n. s. Arb. a. d. kaiserl. Gesundheitsamte. 

1904. xxi p. 42. 
Idem. Beitrag zur. Entamoeba-Frage (Entamoeba williamsi) Arch. f. Protistenk 

1911, xx, p. 345. 

Idem. Zur Kenntnis der Entamoeba. Arch. f. Schiffs-u. Tropenhyg. 1912, 16, I. 

P. 30. 
Idem. Weitere Beitrag zur. Kenntnis d. Entamoeben. VI. Arch. f. Protistenk. 

1912. xxvi, p. 241. 

Schaudinn, F., Untersuch. u. d. Fortpalnzung d. Rhizopoden. Arb. a. d. Kaiserl. 

Gesundheitsamte, 1903, xix, p. 547. 
Sistrunk, W. E., Intestinal Parasites found in Individuals Residing in the 

Northwest. Jour. Amer. Med. Assoc. 1911. lvii, p. 1507. 
Stiles, C. W., The Presence of Entamoeba histolytica and Entamoeba coli In 

North Carolina. Public Health Reports. Washington, xxvi, 1911, p. 1276. 
Strong, R. P., and Musgrave, W. E., Etiology of the Dysenteries of Manila. 

Ann. Rep. Surg. General, U. S. Army, 1900. p. 251. 
Vedder, E., An Examination of the Stools of 100 Healthy Individuals etc., Jour 

Am. Med. Assoc. 1906, xxvi, p. 870. 
Viereck, H., Stndien ueber die in den Tropen erworbene Dysenterie. Arch. f. 

Schiffs-u Tropenhyg., 1907. xi. Beiheft. I. P. 1-41. 
Vivalidi. Le Amebe della Dissenteria. La Riforma Med. Naples. 1894, x, p. 147. 
Walker, E. L., The Parasitic Amebae of the Intestinal Tract of Man and other 

Animals. Jour. Med. Research, 1908, xvii, p. 379. 
Idem. A Comparative Study of the Amebae in the Manila Water-Supply, etc., 

Phil. Jour. Science. Sec. B. 1911, vi, p. 259. 
Wellman, Creighton., Personal Communication. 

Wells, R. T., Aerial Contamination as a Fallacy in the Study of Amoebic Infec- 
tions by Cultural Methods. Parasitology, 1911, iv, p. 204. 
Werner, H., Studies Regarding Pathogenic Amoebae. Indian Medical Gazette. 

1909, xliv, p. 241. 
Whitmore, E., Parasitare and freilebende Amoben aus Manila and Saigon. Arch. 

f. Protistenk. 1911. xxiii, p. 70. 


Whitniore, E. Studien ueber Kultur amoeben aus Manila. Arch. f. Protistenk., 

1911, xxiii, p. 81. 
Williams, Anna., Pure Cultures of Amoebae Parasitic in Animals. Jour. Med. 

Research. 1911, xxv, p. 263. 
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Abt. p. 638. 
Zaubitzer. Studien ueber Strohinfus., amoebae. Arch. f. Hyg., 1901. xlii, p. 




Dr. S. T. Darling, Chief of Laboratory, Isthmian Canal Commission, Ancon, 

Canal Zone. 

The identification of the entamoeba that causes dysentery and liver 
abscess in Panama has recently been placed on a satisfactory basis, 
since two of the members of the hospital staff have given special 
attention to the subject, and have had referred to them for diagnosis 
all cases of entamoebic dysentery. Formerly, each doctor diagnosed 
the cases in his own ward, and there was no uniformity in the identi- 
fication of entamoebae, each man determining for himself whether in 
a given case the entamoeba was E. coli or E. histolytica. 

Influenced by the work of Schaudinn and Craig, until a year ago 
I regarded all pathogenic forms as E. histolytica. In August, 1911, 
a careful study of the entamoebae found in clinical cases of enta- 
moebic dysentery and entamoebic liver abscess was begun, and 
observations since then have led me to be of the opinion that the only 
pathogenic form in this region is E. tetragena (Viereck.). 

Having ample facilities for the collection of material from clinical 
cases, autopsies and the operating room, and for animal experi- 
mentation attempts we're made to determine the specific characters 
of the entamoebae so collected. 

Methods of examination : 

1. Fresh and moist-chamber preparations, and those stained in- 
travitam with gentian violet. 

2. Wet-fixed preparations, stained with haematoxylin, Romo- 
nowsky modifications, and various other stains. 

3. Dry-fixed preparations, stained by modifications of the Ro- 
monowsky method. 

4. Animal inoculations and feeding experiments. 
Examination of fresh preparations: 

It was found that very few of the published descriptions of enta- 
moebae were sufficiently helpful as guides for the purposes of identi- 
fication ; in fact, every step required to be specially worked out, and 
clinical and morphological data correlated with animal experi- 


Take the questions of refractility of the ectoplasm and the color 
of the cytoplasm. It seems to me that refractility is very largely a 
question of the age of the entamoeba, or its relation to encystment, 
without regard to species. I have found, in cultures of free living 
forms, that the younger amoebae were not very refractile, while those 
approaching the period of encystment were quite refractile. In a 
fatal case I found that large trophozoites deep in the submucosa in 
the floors of ulcers were very slightly refractile, while many of the 
smaller entamoebae, in the more superficial sloughs, were highly 
refractile, yet they were representatives of one species. In some 
clinical cases all the forms seen were highly refractile, many con- 
tained chromidia, and were the precursors of the small generation 
from which the cysts develop. In other cases all the entamoebae 
were finely granular, contained no erythrocytes, and were not refrac- 
tile. I have never seen, either with natural or artificial illumination, 
the green or gray tints noted by several writers, and it does not seem 
to me that stained specimens bear out the notion that green color 
is due to lysed erythrocytes, for the latter are held intact for a consid- 
erable period in the endoplasm, and disappear by condensation and 
erosion, while retaining their staining characters. I should say that 
all observations were made with artificial light, transmitted through 
blue glass, and I wish to call attention to the necessity of using some 
such uniform method of illumination, for the difference in illumina- 
tion between light derived from a blue sky, or from white clouds, 
makes their use as sources of light uncertain, and gives inconstant 
pictures usually not noted by the observer. The resulting errors may 
be eliminated by the use of artificial light. 

The nucleus is said to be inconspicuous in the pathogenic enta- 
moeba in fresh preparations, but I have not always found this to be 
the case when artificial light has been used. It is true that in many 
individuals, or in all the individuals in some cases, the nucleus can 
not be made out in fresh preparations. But when one learns to rec- 
ognize the nucleus nothing within the trophozoite is more conspicu- 
ous. The refractile granules or masses of peripheral chromatin 
stand out with great prominence and may be followed with ease as 
the entamoeba moves. 

The presence of an ectosarc is very constant in the trophozoites of 
the pathogenic form, and is an important feature for differentia- 
tion from E. coli. 

While, in most cases, it is true that all entamoebae detected in stools 
associated with pus blood and mucus are pathogenic, it is not this 
type of case that presents difficulties. The puzzling cases are those 
in which entamoebae are detected in fluid stools containing mucus, 
or in semisolid or formed stools unassociated with blood or pus, but 


which it is necessary to diagnose at once, so that treatment may be 
started energetically. 


As an aid to rapid diagnosis, I have used, with some success, gen- 
tian violet as an intra vitam stain. The stain is used in the concen- 
trated fluid form, or diluted with an equal amount of water, and 
is either added to the flake or mucus or drawn under the cover slip, 
and the preparation examined immediately. While many indi- 
viduals become overstained or remain understained, usually they 
will gradually take up the stain in such a manner that the pe- 
ripheral chromatin, the centriole and karysome in E. tetragena 
stand out with almost the clearness and definition of well-stained 
hematoxylin preparations fixed in the wet way, and differentiation 
from E. coli is easy. I have tried several basic stains, but none is so 
good as gentian violet for intravitam staining. Even when the 
trophozoite is very refractory to the stain, as in the small generation, 
and in the forms which contain chromidia, the nucleus for some 
reason will become more refractile and conspicuous. The nonre- 
fractile trophozoites take up the gentian violet rapidly, while cysts 
and the refractile forms take up the stain slowly. 

Haematoxylin-stained preparations were made from those fresh 
films which contained a sufficient number of entamoebae to warrant 
staining and study. The cover slip was removed, and both slip and 
slide were fixed in Schaudinn's bichloride alcohol, or in Zenker's 
solution diluted one-fourth and one-eighth, as the full-strength solu- 
tion causes artefacts in the nucleus. Several haematoxylin stains 
were used and particularly clear pictures were obtained with Mal- 
lory's phosphotungstic acid haematoxylin, with the modification 
that the films were not given a preliminary treatment with oxalic 
acid or permanganate, but were placed over night in the haema- 
toxylin, and then differentiated with very dilute permanganate. This 
is a shorter way of using phosphotungstic acid haematoxylin, and 
gives excellent results. 

Fresh and wet-fixed preparations were controlled or compared 
with others stained after dry fixation by some modification of the 
Romanowsky stain. The films were thoroughly dried, then stained 
with Hasting's stain, overstained with Giemsa's stain, and differ- 
entiated with ammoniated alcohol. It was observed that the de- 
scriptions of pathogenic entamoebae, as well as figures used to illus- 
trate them in the literature, did not correspond with the results ob- 
tained in well-differentiated films stained by the method just de- 
scribed. And it is believed that descriptions in the literature based 
on films stained in the usual way that had not been sufficiently dif- 
ferentiated are not as exact as they might be. Romanowsky stains 


have a tendency to overstain, just as haematoxylin does, though not 
so intensely as the latter, and this overstaining must be corrected 
by the use of a differentiating agent. 

It has been my practice to stain in the following way: Fresh cover- 
slip preparations containing a sufficient number of entamoebae to 
warrant staining and study, or those intended for diagnosis, are made 
into smears by sliding off the cover slip and thoroughly drying both 
slip and slide, after which each is stained with Hasting's stain for 15 
minutes. Satisfactory films are then overstained with Giemsa's stain 
until the film has a diffuse reddish purple tint. The film is then 
plunged into 60 per cent ethyl alcohol containing about 1 per cent of 
water of ammonia (10 per cent), and differentiated in this, washed 
in water, and controlled by the microscope until the purple substance 
of the nucleus and the blue color of the cytoplasm are strongly con- 
trasted. The film when properly differentiated has a blue violet 
color. If the film has been greatly overstained, it is treated with a 
momentary douche of 95 per cent alcohol. Beautiful pictures are 
obtained in this way, but, what is of more importance, the various 
figures displayed by the purple staining substance (karyosome?) 
can be noted and followed with ease. This purple staining sub- 
stance, in the nucleus of Entamoeba tetragena in dried-fixed films, 
represents only a portion of the nucleus, as the centriole and periph- 
eral chromatin do not stain purple by the above method. The pur- 
ple staining substance in the nucleus of E. tetragena frequently 
appears as a ring, or as a reticulum, or scattered granules. Its phases 
do not appear to have been accurately described, but have been con- 
fused with the appearances presented in wet-fixed films when basic 
stains have been used. 

Here I wish to call attention to certain errors of interpretation 
which I believe have resulted from the failure to properly distin- 
guish between the purple staining substance, or karyosome of the 
nucleus in Entamoeba tetragena in dry-fixed films, and the nuclear 
substance which stains with basic stains in wet-fixed preparations. 
For example: cuts showing the purple chromation of the nucleus of 
E. histolytica represented by Craig and illustrated in its proper color, 
have been used by other writers and figured in terms of haematoxylin, 
or black and white, without explaining that the black in the figure 
represents the purple staining substance of dry-fixed Romanowsky 
preparations. Dry-fixed stained films should never be confused with 
those stained after wet fixation, for the pictures are different in each 
case, and the mistake should never be made of attempting to trans- 
late one into the other. In dry-fixed films the permeability of the 
entamoebae to stains apparently has been profoundly modified, for 
the centriole and the peripheral chromatin do not take or retain the 


purple stain. The karyosome alone retains the purple stain, while 
the remainder of the nucleus stains faintly blue, sometimes revealing 
the achromatic granules of uniform size which appear to form part 
of its structure. 

Feeding and inoculation experiments: 

A number of kittens, cats, dogs, and monkeys have been fed by 
mouth, or inoculated per rectum, with cysts and trophozoites of 
Entamoeba tetragena. When tetragena cysts have been fed to half- 
grown cats, there has resulted, not the typical entamoebic 1 colitis, 
such as is usually described in the literature, but an enteritis, and, 
in this lesion in the ileum, trophozoites have been found which, 
though arising from tetragena cysts, had the morphology not only of 
E. tetragena, but of E. histolytica and E. nipponica. Now, as ma- 
terial which, from its history and microscopical appearance, was cer- 
tainly a pure culture of E. tetragena cysts was used in the experi- 
ment, and as the various forms appeared in the cat's intestines, I am 
led to believe that the large vegetative trophozoites, described as 
E. histolytica and E. nipponica by various writers, are nothing more 
than the large trophozoites in the first place, and atypical or 
degenerate form of E. tetragena in the latter, and I am confirmed in 
this opinion by never finding in my cases any of the perpetuating 
forms described by Schaudinn and Craig for E. histolytica. In 
one fatal case of tetragena infection, I observed from autopsy ma- 
terial many trophozoites that protruded psudopodia not unlike those 
figured by Craig for E. histolytica. Their extremities were re- 
fractile and appeared to contain a round, spore-like body; yet, 
when these coverslip preparations were fixed immediately and 
stained with haematoxylin and by Romanowsky, the picture pre- 
sented was that of E. tetragena, and the spore-like bodies had dis- 
appeared. In studying a strain of E. tetragena in cats, following 
rectal injection of trophozoites, I found at the fourth remove in dry 
fixed preparations a great many trophozoites, the peripheries of 
which contained one or several labose projections, which were very 
frequently deeply stained blue or contained a nucleus and suggested 
strongly the descriptions of E. histolytica by Craig, but these were 
artefacts ; for, in wet- fixed haematoxylin preparations from the same 
coverslip preparation, the picture was that of E. tetragena; and 
associated with these trophozoites were several uninucleated tetra- 
gena cysts. If only the dry-fixed films had been studied in this case, 
they might easily have been described as E. histolytica. 

With reference to rectal inoculation of trophozoites, infection 
occurs within a few days (5 to 8) if the strain is not too aged or 
near the stage of encystment; while, by mouth feeding, the dura- 
tion is longer (12 days). In this, my experiments have not paral- 
leled those of other writers. It is difficult to explain this; but I may 


say that, after several unsuccessful attempts to infect very young 
kittens and adult cats, I subsequently only used kittens weighing 
about 700 grams. 

Animal experimentation is of very great value in studying the 
variation in a given strain. In a strain in kittens recently, I have 
been able to watch senility gradually developing from week to week, 
the entamoebae becoming reduced in size, filled with chromidia, and 
ultimately becoming encysted. 

The comparative study of staining and fixing agents has brought 
out some very interesting information. The very marked differences 
presented by dry-fixed and wet-fixed stained preparations have been 
referred to. Phosphotungstic acid haematoxylin gives varying pic- 
tures, depending on the fixative. More information of the structure 
of the nucleus is obtained by the use of this stain, after fixing with 
diluted Zenker's fluid (one-eighth and one-fourth) and Flemming's 
fluid. The karyosome is not so well transfixed when fixed with 
Merkel's, Hermann's, or Schaudinn's fluid. In wet-fixed films stained 
by Romanowsky, it was never possible to stain the trophozoites 
exactly like the tissue cells near by. When stained by Giemsa's 
method, and differentiated in acetone xylol, the peripheral chromatin 
usually stained blue, while the centriole and nuclear sap stained 
pink or red, the tissue cells nearby displayed purple staining sub- 
stance throughout the nucleus. 

It was possible, in several cases, to study first the tissue destroying 
trophozoites, later the small generation, and, finally, during con- 
valescence and after apparent recovery, the cysts, although in prac- 
tically all cases that received energetic medication, the small genera- 
tion and cysts did not appear. 

The detection of crysts in convalescent and recovered cases is 
most important, for it is the cyst and not the trophozoite which is 
the infecting agent and makes the host of the former a " carrier." 
The identification of tetragena cysts is usually easy in stained prepa- 
rations, and should present no difficulties in fresh films, yet the cysts 
are so small (12 to 15 microns in diameter) that they have fre- 
quently been mistaken for monad or coli cysts, or fat droplets, or 
possibly mononuclear leukocytes. When in doubt, and when the 
number of cysts was too small to risk loss by fixation and staining, 
I have vaselined the preparation, or kept it in a moist chamber; and, 
if the cyst was homogeneous at first, after one or two days, one, two, 
or four nuclei became distinctly visible. Tetragena cysts are more 
commonly detected in neglected cases which have partly recovered 
from entamoebic dysentery who may have diarrhoea or whose stools 
are solid; and I have found cysts in a case that had been insuffi- 
ciently treated by means of rectal injections. It would seem that 
if a case of dysentery is treated early and energetically, the tropho- 


zoites are at once driven from the field, leaving none to develop into 
the drug-resistant small generation from which the cysts arise. This 
it will be seen is analogous to the rational treatment of malaria, in 
which the asexual generation is destroyed at once by large doses of 
quinine, thus destroying all the forms from which the gametes arise. 

In acute or new infections, or in very active lesions, many of the 
trophozoites are of large size — 30 to 60 microns in diameter. As the 
strain grows older, it often becomes reduced in size, the trophozoites 
measuring from 12 to 24 microns in diameter. These forms fre- 
quently contain coarse blocks of chromidia, and they constitute the 
" small generation." During convalescence, and after apparent 
recovery, there appear small trophozoites, 12 to 15 microns in diam- 
eter, and associated with them are cysts and four nucleated schizonts. 
If relapse occurs with symptoms of colitis, large trophozoites make 
their appearance again, and the cysts will have disappeared. Thus, 
during the progress of a case of tetragena dysentery, one will see at 
first large trophozoites, many or all of them having the characters 
described for E. histolytica by Schaudinn and Craig, and one will 
see later, if the case has been a neglected one, the small generation 
with cysts, of which there is no better description extant than that 
in Elmassian's paper on this form, which he has called E. minuta. 

If there is a sufficient number of cysts, they may be fed by mouth 
to young cats, and it may be possible to recover from their bowel 
lesions trophozoites having not only the characters of E. tetragena, 
but of E. histolytica and E. nipponica as well. Or, if in any 
given case of tetragena dysentery, in which the trophozoites are of 
the histolytica type, they be injected rectally into a young cat, and 
the strain carried on by subsequent rectal inoculation into other cats 
at the time the infected animal dies, so as to prolong the vegetative 
phase of division, then it will be seen that the histolytica -like tropho- 
zoites become reduced in size, filled with chromidia, and, at the 
fourth or fifth remove, it is possible to find uninucleated tetragena 
cysts. The nucleus of the trophozoite meanwhile has taken on a 
typical tetragena appearance with a prominent karyosome. It is 
now impossible to infect other cats per rectum with this material. If 
we make dry-fixed Romanowsky-stained smears of material con- 
taining these typical tetragena trophozoites, they will occasionally 
present the morphological peculiarities of E. histolytica described 
by Craig, and we are thus able to correlate most of the observations 
of Schaudinn, Craig, Elmassian, and Koidzumi, and state that there 
is almost certainly but one pathogenic entamoeba, and that one is 
E. tetragena. 

1 Since reading the paper (December 9), I have provoked entamoebic colitis 
in a kitten fed with tetragemi cysts that had been in the moist chamber 54 



Prof. Creighton Wellman. New Orleans : I may add to the refer- 
ence to my animal experiments made in Capt. Craig's paper that since 
the data sent him I have made a few more feeding and rectal injec- 
tion experiments in kittens, using both what we regard as ooli and 
histolytica. The protocols of these run about as those sent him, no 
lesions resulting from coli and frequently following histolytica infec- 
tions. Perhaps I ought 'to add that the animals employed were care- 
fully and repeatedly examined for some time before the experiments 
were begun. 

Capt. Charles F. Craig, Medical Corps, United States Army: I 
have been much interested in the valuable paper of Dr. Darling 
regarding the species of entamoeba producing dysentery in Panama. 
Dr. Darling believes, from his observations, that Entamoeba tetra- 
gena is the only pathogenic amoebae present there, but I have found 
what I believe to be Entamoeba histolytica, as well as Entamoeba 
tetragena, in properly stained preparations sent me by Dr. James for 
my opinion. As I have stated in my paper, until it can be shown 
that the peculiar method of reproduction described by Schaudinn 
as budding or gemmation, and afterward confirmed by myself in 
both living and stained entamoeba, occurs in Entamoeba tetra- 
gena as well as Entamoeba histolytica, I must consider the two as 
distinct species, despite the fact that at certain stages of development 
the nuclear structure of tetragena resembles that of histolytica. 
Though there is a resemblance, I will say that I have seen Dr. Dar- 
ling's preparations, and even in those entamoeba presenting the 
histolytica type of nucleus, the centriole is much larger and the 
nuclear membrane much thicker than in the true histolytica. As 
regards the spores described by Schaudinn and myself and others 
being artefacts, I would say that I am sure that such a mistake could 
not be made, especially when we both observed the process in the 
living parasite. I am quite sure that I know artefacts when I see 
them, and I am still more sure that Schaudinn did. This supposi- 
tion proves, to my mind, that Dr. Darling has not handled histo- 
lytica, or, if so, has failed to recognize the species, for no one 
could mistake the histolytica spores for artefacts. They are small, 
oval bodies, measuring on the average about 4 microns in diameter, 
somewhat bile stained, and having a single or double contoured mem- 
brane, and they may be very easily overlooked by one who has not 
once had then pointed out. They show no structure on staining 
because of the deepness of the staining and the impossibility of 
extracting the stain. 


Specimens of both histolytica and tetragena frequently occur in 
the same case, and this does not appear to be considered by Dr. Dar- 
ling in his paper. I have repeatedly seen mixed infections with 
these two species, as well as single infections. 

The process of cyst formation in Entamoeba tetragena is distinc- 
tive, four nucleated cysts being produced, but such cysts never occur 
in the developmental cycle of histolytica. I have followed scores of 
cases of pure histolytica infection through every stage of the disease, 
from the acute attack until recovery appeared complete, and through 
several relapses, and have never observed a single tetragena cyst, 
the only forms being the minute spores which are found during heal- 
ing and apparent recovery. Dr. Darling states that in his cases 
showing amoebae having the histolytica type of nucleus cysts are 
observed when the patient improves. In this case he may have been 
handling a mixed infection with histolytica and tetragena, or the 
amoebae were all tetragena, some of them showing a nucleus resem- 
bling histolytica, but which, as I have already said, is not identical 
with the true histolytica nucleus. In addition, Dr. James, one of 
Dr. Darling's colleagues on the Isthmus, in a letter received by me 
only a day or two ago, states positively that the infections he regards 
as being due to histolytica do not show four nucleated cysts at any 
time in their course, and that in addition the clinical symptoms of 
histolytica infections are different from those of tetragen infections. 

As regards the examination of entamoeba by natural and artificial 
light, I would say that I am familiar with the appearance of the 
organisms under both methods of illumination, but daylight is cer- 
tainly preferable in work with these parasites, provided the light 
comes from the north. The nucleus of histolytica very frequently 
is invisible in the living parasite, no matter what method of illu- 
mination is used. 

In his paper Dr. Darling states that he was not able to produce the 
typical lesions of dysentery in the colon of kittens with Entamoeba 
tetragena, but instead a severe enteritis, the condition being most 
marked in the ileum. This is a totally different result than is 
obtained with experimental infections with Entamoeba histolytica, 
in which the lesions are typical and almost always confined to the 
large intestine, very seldom being marked much above the ileo-caecal 
valve. These observations of Darling would apparently show that 
the lesions in cats produced by tetragena differ very markedly from 
those produced by histolytica. 

The presence of four nuclei in the vegetative stage of tetragena, 
noted by Dr. Darling, is most interesting, as the process of schizogony 
has not been definitely proved in this species, and these observations 
would appear to prove that it occurs. 


Dr. Darling's remarks concerning the morphological differences in 
entamoebae, caused by dry and wet fixation and by different methods 
of staining, are important, but, I think, fully recognized by all who 
have worked for any length of time with these parasites. 

I agree with Prof. Stiles in what he says regarding the transmission 
of entamoeba by water. I do not believe that these parasites are thus 
transmitted to any great extent. I see no theoretical objection to 
Dr. Stiles's theory of the transmission of the spores and cysts by the 
fly ; but I do not think that this insect is responsible in the Philippine 
Islands, for the fly is a rare insect there, as everyone knows who has 
traveled through the country. I am inclined to believe that contact 
infection and dust infection are greater sources of the disease than 
fly transmission, at least in the Philippines. 

Dr. Samuel T. Darling: It is possible that my observations on 
the morphology of E. tetragena, and the observations recorded by 
Dr. Craig on the developmental phase of E. histolytica, in which 
spore formation by budding is described may be harmonized. The 
nonencysted forms of E. tetragena, showing four nuclei and division 
of the nucleus into four daughter nuclei, as Dr. Craig has suggested 
to me, may be identical with the forms noted by Dr. Craig in E. his- 
tolytica, i. e., the nuclei in the four nucleated naked forms may be- 
come pinched off to form new individuals. Unfortunately, at this 
time no observations tending to confirm this view have been made. 
There is something very characteristic about the pathological fea- 
tures of infection by E. tetragena, and I believe that, if there is more 
than one pathogenic entamoeba, we should expect to find more than 
one type of lesion. This does not seem to be the case, for the lesions 
caused by E. tetragena are unique and unvarying, and they are 
exactly like the lesions described elsewhere in the tropics as being 
caused by E. histolytica. In my opinion, the pathogenic entamoeba 
is one having the essential characteristics of E. tetragena with four 
nucleated cysts. 

The statement by Dr. Stiles that E. coli disappears from the stools 
after the administration of flowers of sulphur interests me a great 
deal. As some of you may know, the mode of treatment for enta- 
moebic dysentery at Ancon Hospital is the administration of large 
doses of bismuth. Stools from cases treated in this way by means of 
bismuth contain from 10 to 12 per cent by weight of bismuth sub- 
nitrate. The stools are frequently quite black, and, upon microscopic 
examination, I found the color to be due partly to a deposit of black 
bismuth sulphide on the surfaces of the white bismuth subnitrate 
crystals, and in part to the staining of microcococci and bacteria, 
for they had assimilated the bismuth salts into their substance, and 
66692— vol 2, pt 1—13 12 


this had become changed into black bismuth sulphide. The stools 
were usually free from fetid odor and from odors suggestive of 
hydrogen sulphide. At the same time, I confirmed the observation 
that trophozoites of E. tetragena usually disappear from faeces 
within two or three days after the administration of large doses of 
bismuth subnitrate. It would thus appear that while, according to 
Dr. Stiles's observations, E. coli is removed by administration of 
sulphur, E. tetragena disappears coincidently with the abstraction 
and locking up of sulphur in the bacteria and intestinal content by 
the bismuth subnitrate. 



By Howard Ceawley, Assist. Zoologist, United States Department of Agri- 
culture, Washington, D. C. 

The following list, which is believed to contain all the names which 
have been applied to parasitic amoebae, is arranged alphabetically so 
far as the specific names are concerned. Under each species name is 
placed the one or more generic names with which the species name 
has been combined. With one exception, these combinations refer 
to the same organism; thus, histolytica has been combined with five 
different generic names, but each one of these five combinations re- 
fers to the same organism. The exception is the species intestinalis. 
Walker uses the name Ameba intestinalis (which Doflein puts into 
the genus Entamoeba), but states it is not the same form as that 
named Amoeba intestinalis by Blanchard. 

It has not been considered advisable to attempt a determination 
of the status of these various forms according to the International 

The titles and places of publication of the references given will be 
found in the paper by Dr. Albert Hassall, entitled " Bibliography of 
parasitic amoebae." 


Amoeba Brumpt, 1910, p. 32. 

Entamoeba Hartmann in Hartmann & Prowazek, 1907, p. 312 footnote. 

Entamoeba Fantham & Porter, 1911, p. 626. 

Amoeba Celli & Fiocca, 1894 b, p. 439. 

Entamoeba Noller, 1912, p, 195. 

Amoeba Biitschli, 1878 a, pp. 273-277. 

Endamoeba Leidy, 1879 a, p. 300; 1879 k, p. 205. 
• Entamoeba Doflein, 1909, p. 499. 

Amoeba Calandruccio, 1890 a, p. 99. 

Entamoeba Casagrandi & Barbagallo. 1S97. p. 163. 




Amoeba Doflein, 1901 a, pp. 17-18. 
bo vis 

Amoeba Liebetanz, 1905 a, p. 314. 

Entamoeba Doflein, 1909, p. 499. 

Loeschia Chatton, 1912, p. 182. 
? de Beaurepaire Aragao, 1912. 


Amoeba Steinberg, 1862 a. 

Entamoeba Prowazek, 1904, p. 42. 

Entamoeba Prowazek, 1912, p. 245. 

Amoeba Grassi, 1882 a, pp. 185-187. 

Amoeba Porter, 1909, pp. 32-41. 

Amoeba Graham, 1899 a, p. 477 (eiliata, p. 515, ciliaria renamed). 

Ameba Walker, 1908, pp. 429, 442 (spelled copayae, p. 429). 

Entamoeba Sluiter & Swellengrebel, 1912, pp. 23, 24. 

Amoeba Loesch, 1875 a, p. 210. 

Entamoeba Schubotz, 1905 b, p. 34. 

Entamoeba Scbandinn, 1903 a, p. 564. 

Loeschia Chatton, 1912, p. 181. 
coli communis 

Amoeba Kruse, 1896 a, p. 613. 
coli dysenteriae 

Amoeba Doflein & von Prowazek, 1903, p. 918. 
coli dysenterica 

Amoeba Jansen, 1898 a, p. 134. 
coli dysenterici 

Amoeba Kruse, 1896 a, p. 613. 
coli felis 

Amoeba Quincke & Roos, 1893 a, p- 1093. 
coli hommis 

Amoeba Kuenen, 1909, p. 564. 
coli incapsulata 

Amoeba Maggiora, 1891, p. 725. 
coli intcstini vulgaris 

Amoeba Fenoglio, 1904. p. 252. 
coli mitis 

Amoeba Quincke & Roos, 1893 a, p. 1093. 
coli nipponica 

Entamoeba Walker, 1911, p. 279. 
coli vulgaris 

Amoeba Ziegler, 1895 a, p. 717. 

Amoeba Rivolta & Delprato, 1881a 

Ameba Perroncito, 1882a, p. 95. 



Amoeba Metcalf, 1910, pp. 308-310. 

Amoeba Braun, 1883 a, p. 11. 

Entamoeba Froscb, 1909, p. 191. 

Amoeba Celli & Fiocca, 1894 b, p. 438. 

Amoeba Fenoglio, 1904, p. 251. 

Amoeba Councilman & Lafleur, 1891 a, p. 405. 

Entamoeba Craig, 1905, pp. 245-289. 

Amoeba Pfeiffer, 1888 c, p. 662. 

Entamoeba Thornburgh, 1908 a, pp. 55, 56. 
ent erica 

Ameba Walker, 1908 a, pp. 429, 443. 
febris flavae 

Amoeba Tbayer, A. E., 1907 a, p. 49. 
febris tertianae 

Amoeba Kruse, 1896 a, p. 673 (name credited to Golgi). 

Ameba Walker, 1908 a, pp. 386, 429. 

Amoeba Quincke & Roos, 1893 a, p. 1093. 

Amoeba Casagrandi & Barbagallo, 1897 a, p. 586. [No evidence that this is 
a parasite.] 

Ameba Walker, 1908 a, pp. 429, 444 (spelled galloparvonis on p. 429). 

Amoebea Gros, 1849 a, p. 555. 

Amoeba Braun, 1895 b, p. 44. 

Entamoeba Castellani & Chalmers, 1910, p. 214. 

Amoeba Celli & Fiocca, 1894 b, p. 436. 

Entamoeba von Prowazek, 1912, p. 243. 

Amoeba Castellani, 1904, p. 509. 

Entamoeba Castellani, 1904, p. 507. 

Amoeba Motas, 1906, p. 682 (error for histolytica), 

Amoeba Broido, 1903, pp. 827, 828. 

Endamoeba Hickson, 1909, pp. 82, 83. 

Entamoeba Schaudinn, 1903 a, pp. 564, 570. 

Loeschia Chatton & Lalung-Bonnaire, 1912, pi. 9, facing p. 138. 

Poneramoeba Luehe, 1909, p. 421. 
histolytica dysenteriae 

entamoeba Hara, 1910, pp. 340, 367. 
histolytica tetragina 

Entamoeba Walker, 1911, p. 279. 


ho minis 

Ameba Walker, 1908 a, pp. 429, 444. 

Entamoeba Casagrandi & Barbagallo, 1897, p. 163. 

Paramoeba Craig, 1906, p. 214. 

Endamoeba Schubotz, 1905 b, p. 34. 

Amoeba Jelks, 1910, p. 55. 

Amoeba Wesener, 1892 a, p. 541 

Amoeba R. Blancbard, 1885 g, p. 15. 

Ameba Walker, 1908 a, pp. 414, 429. 

Entamoeba Doflein, 1909, p. 508. 
intestinalis vulgaris 

Amoeba Eicbborst, 1901 a, p. 292. 
intestini vulgaris 

Amoeba Quincke & Roos, 1893 a, p. 1093. 

Amoeba Fenoglio, 1904, pp. 251, 252. 

Endamoeba Hickson, 1909, p. 83 (error for miurai), 

Amoeba von Mereschowsky, 1878 a, p. 204 

Amoeba Doflein, 1901 a, p. 30. 

Entamoeba Doflein, 1909, p. 506. 

Amoeba Hartmann in Hartniann & von Prowazek, 1907, p. 314. 

Vahlkampfia Cbatton, 1912, p. 112. 

Amoeba (Entamoeba) Fantbam, 1910, p. 702. 

Amoeba Letulle, 1908, pp. 256-266. 

Amoeba Pfeiffer, 1891 a, p. 211. 

Amoeba Cell! & Fiocca, 1894 b, p. 486. 
lobosa coli 

Amoeba Celli & Fiocca, 1894, b, p. 436. 
lobosa gruberi 

Amoeba Wuelker, 1911, p. 592. 
lobosa guttula 

Amoeba Celli & Fiocca, 1894 b, p. 436. 
lobosa oblonga 

Amoeba Celli & Fiocca, 1894 b, p. 436 (name credited to Sclimarda). 

Amoeba Craig, 1912, pp. 1, 25-30. 

Entamoeba Lesage, 1908, p. 105 
malariae (hominis) 

Amoeba Sakbarov, 1892 a. 


malariae fcbris quartanae 

Amoeba Kruse, 1896 a, p. 672 (name credited to Golgl). 

Entamoeba Kartulis, 1906, p. 356. 

Amoeba Smith, 1895 a, pp. 1-38. 

Entamoeba Doflein, 1909, p. 508. 

Amoeba Cole, 1908, p. 297. 

Ameba Walker, 1908 a, p. 446 (error for meleagridis) . 

Amoeba Gedoelst, 1911, p. 33. 

Entamoeba Elmassian, 1909, p. 335. 

Loeschia Chatton, 1912, p. 182. 

Amoeba Cramer, 1896 a, p. 143. 

Amoeba Ijima, 1898 a, p. 85. 

Endamoeba Hickson, 1909, p. 83 (spelled iurai, obviously a misprint). 

Entamoeba Castellani & Chalmers, 1910, p. 214. 

Amoeba Gedoelst, 1911, p. 33. 

Entamoeba Smith & Weidman, 1910, pp. 285-298. 

Entamoeba Raff, 1912, pp. 340-351. 

Amoeba Chatton, 1909, p. 690. 

Amoeba Grassi, 1882 a, pp. 181-182. 

Entamoeba Hartmann, 1907, p. 143. 

Proctamoeba Alexeieff, 1912, p. 64. 

Ameba Walker, 1908 a, pp. 429, 447. 

Entamoeba Doflein, 1911, p. 579. 

Amoeba Gedoelst, 1911, p. 33. 

Entamoeba Koidzumi, 1909, p. 650. 

Entamoeba Castellani, 1908, p. 102. 

Amoeba Celli & Fiocca, 1894 b, p. 436 (name credited to Schmarda). 

Entamoeba Billet, 1907, p. 217 (error for undulans). 
paedophthora (variously spelled). 

Amoeba Caullery, 1906, p. 267. 

Entamoeba Castellani & Chalmers, 1910, p. 215. 

Vahlkampfia Chatton, 1912, p. 112. 

Amoeba Lendenfeld, 1885 a, pp. 35-38. 

Amoeba Gedoelst, 1911, p. 32. 

Entamoeba Gauducheau, 1907, pp. 486--487. 



Amoeba Grassi, 1881, p. 354. 

Entamoeba von Prowazek, 1912, p. 246. 

Entamoeba von Prowazek, 1912, p. 274. 

Amoeba Artault, 1898, pp. 275-277. 

Entamoeba Castellani & Chalmers, 1910, p. 214. 

Ameba Walker, 1908 a, pp. 429, 447? 

Entamoeba Hartmann, 1907, p. 143. 

Amoeba Grassi, 1879 m, p. 446. 

Entamoeba Dobell, 1908, p. 428. 

Proctamoeba Alexeieff, 1912, p. 66. 

Entamoeba Castellani & Chalmers, 1910, p. 215 (error for ranarum). 

Amoeba Celli & Fiocca, 1894 b, p. 439. 

Amoeba Mayer, 1843 a, p. 11. 

Amoeba Grassi, 1881, p. 354. 

Proctamoeba Alexeieff, 1912, p. 64. 

Entamoeba Lesage, 1908, p. 105. 

Amoeba Celli & Fiocca, 1894 b, p. 437. 

Amoeba Pfeiffer, L., 1891 a, p. 211. 

Entamoeba Hartmann, 1909, p. 209. 

Amoeba Hartmann, 1908, p. 126. 

Entamoeba Viereck, 1907 c, p. 32. 

Loeschia Chatton & Lalung-Bonnaire, 1912, pi. 9 facing p. 138. 

Viereckia (subgenus) Chatton & Lalung-Bonnaire, 1912, p. 142. 

Entamoeba Walker, 1911, p. 276. 

Entamoeba Hartmann in Hartmann & von Prowazek, 1907, p. 312 footnote 
(error for tetragena). 

Amoeba Gedoelst, 1911, p. 33. 

Entamoeba Lesage, 1908, p. 105. 

Amoeba Celli & Fiocca, 1894 b, p. 436 (as variety of Amoeba lobosa; not spe- 
cifically stated to be a parasite). 

Endamoeba Hickson, 1909, p. 83. 

Entamoeba Castellani, 1904, p. 508. 



Ameba Walker, 1908 a, p. 423 (eror for urogenitalis) . 

Amoeba Baelz, 1883 a, p. 237. 

Entamoeba Doflein, 1909, p. 505. 

Amoeba R. Blancliard, 1885 g, p. 15. 

Amoeba Celli & Fiocca, 1894 b, p. 438 (credited to Weisse). 

Amoeba Wuelker, 1911, p. 609. 

Amoeba Roos, 1894 c, p. 391. 

Entamoeba von Prowazek, 1911, p. 349. 

Amoeba Broi'do, 1903, p. 33 (error for jelaginia). 

The several genera named above, with their type species, are given 
in the following list : 

Amoeba proteus. 

Endamoeba blattae Leidy, 1879 a, p. 300 ; 1879 k, p. 205. 
Entamoeba histolytica Schaudinn, 1903 a, pp. 564, 570. 
Loeschia coli Chatton, 1912, p. 110. 
Paramoeba eilhardi Schaudinn, 1896 b, p. 31. 
Poneramoeba histolytica Luehe, 1909, p. 421. 
Proctamoeba synonym of Loeschia. 
Vahlkampfia vahlkampfi Chatton, 1912, p. 112. 


Dr. M. J. S. von Prowazek, Seemannskrankenhaus und Institut fur Schiffs- 
und Tropenkrankheiten, Hamburg, Germany. 

Bei einer Besprechung des Kernaufbaues der parasitischen Amoben 
ist es zunachst notwendig, den innerhalb ziemlich weiter Grenzen 
schwankenden Begriff des Parasitismus dieser Amoeben irgendwie 
abzugrenzen. — Fur eine derartige Begriffsabgrenzung ist in erster 
Linie eine genaue Kenntnis der gesamten biologie der fraglichen 
Organismen, die leider bis jetzt bie den Amoben nur sehr liickenhaft 
bekannt ist, vorbedingung. Aus diesem letzteren Grunde miissen wir 
eine kunstliche Abgrenzung der parasitischen Amoben vornehmen, 
und wir ziehen in den Rahmen unserer Betrachtung nur solche For- 
men ein, deren Weiterentwicklung notwendig an einen Wirt gebun- 
den ist und die daher ausserhalf eines Wirtstieres auf langere Zeit in 
der freien Aussenwelt nicht leben konnen und aus diesem Grunde 
vermutlich nicht oder schwer ziichtbar sind. Auf Grund dieser 
Annahme scheiden aus unserer Betrachung alle Amoben aus, die 


gelegentlich in den Korperhohlen eines Zwischenwirts vorkommen 
knonen — es sind dies alle Amoben des Limaxtypus, wie z. B. Amoeba 
lacertae, die Nagler selbst als einen Saprophyten auf gef asst hatte. 

Bei unserer Untersuchung werden uns hauptsachlich Reprasen- 
tanten der Gattung Entamoeba beschaftigen ; diese Formen sind bis 
jetzt gleichfalls nicht im strengen systematischen Sinne definierbar, 
da wir ihren ganzen Entwicklungszyklus nicht kennen und die Frage, 
ob bei alien eine Autogamie oder Heterogamie bezw. Paedogamie 
vorkommt, das Verhalten ihrer Chromidien u. a. m. definitive noch 
nicht erledigt ist. 

Von den parasitischen Amoben miissen wir ferner diejenigen For- 
men ausscheiden, bei denen der gesamte Kernaufbau noch nicht 
untersucht bezw. noch nicht beschrieben worden ist — denn Angaben, 
dass der Kern rund oder blaschenformig ist und im Zentrum einen 
" Nucleolus " oder ein " Karyosom " enthalt, genugen den Ansprii- 
chen moderner Zytologie nicht mehr. Es sind dies f olgende Amoben : 

(1) Amoeba bovis Liebetanz (hab. Bos taurus). 

(2) Amoebo cobayae n. sp. E. L. Walker " Nucleus circular in out- 
line, but plastic surrounded by a hyaline halo, otherwise homo- 

(3) Amoeba gallopavonis n. sp. E. L. Walker (hab. Meleagris 
gallopavo) . 

(4) Amoeba intestinalis E. L. Walker (hab. Equus caballus, Sus 
scor fa domestica, Felis domestica, Meleagris gallopavo). 

(5) Amoeba kartulisi Doflein (hab. Homo sapiens). 

(6) Amoeba urogenitalis Baelz (hab. Homo sapiens), 

(7) Entamoeba phagocytoides Gauducheau (hab. Homo sapiens), 

(8) Entamoeba undulans Castellani (hab. Homo sapiens). 

(9) Entamoeba nutalli Castellani (hab. Macacus pillatus). 

Die Kernstruktur ist bei folgenden Amoben genauer, wenn auch 
nicht vollstadig bekannt geworden : 

A. Entamoben mit typischem Karyosomkern : 

(1) Entamoeba coli Schaudinn und ihre Varietat Entamoeba wil- 
liamsi Prowazek (hab. Homo sapiens). 

(2) Entamoeba buecalis Prowazek (hab. Homo sapiens). 

(3) Entamoeba histolytica Schaudinn (hab. Homo sapiens). 

(4) Entamoeba tetragena Viereck (hab. Homo sapiens). 

[Falls die " Brutbildung," die Schaudinn bei E. histolytica be- 
schrieben hatte, sich nicht bestatigen sollte und die Tetragenacysten 
tatsachlich in den Entwicklungskreis der Histolytica hineingehoren, 
so muss der Name der spater beschriebenen Ent. tetragena zu Gunsten 
der Entamoeba histolytica verschwinden. Ausser den Angaben 
Schaudinns ware jedoch immer noch die zweite Mitteilung Craigs 
sowie Lesages fur die Selbstandigkeit der Histolytica anzufuhren; 


ausserdem aber der von A. Kuenen und Werner betonte Umstand, 
dass es Amobendysenterien gibt, bei denen Amoben ohne Tetragena- 
cysten mit Histolyticatypus vorkommen.] 

(5) Entamoeba minuta Elmassian, von einigen Autoren als selbst- 
standige Art angezweifelt (hab. Homo sapiens). 

(6) Entamoeba nipponica Koidzumi (hab. Homo sapiens, vergl. 
wie 5). 

(7) Entamoeba hartmanni n. sp. Prowazek (hab. Homo sapiens, 

(8) Entamoeba pitheci Prowazek (hab. Orang-utan). 

(9) Entamoeba polecki Prowazek (hab. Sus scorfa, gelegentlich 
Homo sapiens). 

(10) Entamoeba muris Grassi (hab. Mils). 

((1) Entamoeba testudinis Hartmann (hab. Testudo graeca). 

(12) Entamoeba ranarum Grassi (hab. Rana esculenta). 

(13) Entamoeba aulastomi Noller (hab. Aulastomum gulo). 

B. Entamoeben mit einem Karyosomkern, in dem neben dem 
Karyosomkern noch Chromatinnukleolen (Janicki) vorkommen. 

(14) Entamoeba blattae Biitschli. 

C. Amoben, deren Parasitismus noch unklar ist : 

(1) Chlamydophrys-Leydenia gemmipara (Schaudinn). 

Der Kern der Leydenia ist rund, blaschenformig, besitzt einen mit 
Boraxkarmin, Thionin, Brasilin farbbaren " Pseudonukleolus " und 
eine helle, chromatinfreie, wabig gebaute Kernsaftzone. Kerndurch- 
messer ca. 5 [/., Kernsaftzone f-|j., Kernteilung amitotisch, der 
Pseudonukleolus schniirt sich durch; Kernknospung wurde gleich- 
falls beschrieben (hab. Homo sapiens) in zwei Fallen von Carcinom v. 
Ley den beobachtet. Nach einer spateren Mitteilung Schaudinns ge- 
hort Leydenia zu Chlamydophrys. 

(2) Paramoeba hominis (hab. Homo sapiens) Ch. F. Craig hat 
zuerst bei eigenartigen Diarrhoen in Manila eine Paramoeba beschrie- 
ben und ihre Entwicklungsgeschichte beobachtet. Eine Schilderung 
der feineren Kernstrukturen steht noch aus. 


Bei alien diesen Amoben ist der Kern mehr oder weniger sphaerisch 
rund oder rundlich ; bei Ent histolytica verandert er nach Schaudinn 
unci Hartmann gelegentlich wahrend des Lebens seine Gestalt und 
wird bei der Bewegung passiv leicht verzerrt, exzentrisch verlagert 
und zusammengepresst. Fur den Kern der Ent. blattae nahm 
Schubotz and, dass er gelegentlich aktiv veranderlich werden kann. 
Janicki konnte sich von einer aktiven Beweglichkeit nicht iiberzeugen 
und erklarte mit Mercier die bereits von Biitschli gelegentlich 
beobachteten " geschnabelten " Kerne fur Kernindividuen, die eben 
aus der Teilung hervorgegangen sind. 



Der Dnrchmesser der Kerne schwankt ausserordentlich. Junge 
Amoben von Ent. aulastomi besitzen Kerne, deren Durchmesser 7.5 p 
betragt, grosse, erwachsene Formen erreichen einen Kerndurchmesser 
von 10 \l. Bei Ent. blattae fand Schubotz den Durchmesser kugeliger 
Kerne 15-20 \l 3 die obere Grenze dlirfte 30 ^ nicht iiberschreiten. 
Der Kern von Ent. testudinis betragt 12.5 oder 11.5 zu 15 jjl. Der 
Kern von Ent. ranarum hat nach Dobell einen Durchmesser von 4.4 \l. 
Bei Ent. hartmanni kommen in ein und derselben Zyste neben grossen 
Kernen auch kleine Kerne vor. 


(1) Kernmembran. 

Alle Entamoben besitzen wahrscheinlich eine Kernmembran. Bei 
Ent. coli, buccalis, tetragena, minuta, nipponica, hartmanni, pithed 
und polechi kommt eine gleichmassig ausgebildete Kernmembran 
vor, bei Entamoeba testudinis ist der Kern gegen das Plasma durch 
eine deutliche, doppelkonturierte, derbe Kernmembran abgegrenzt. 
Auffallend dick ist die Kernmembran bei Ent. blattae (1-2 \l) und 
Schubotz konnte in ihr zwei Strukturschichten unterscheiden ; die 
innere Schicht soil dunner sein als die aussere. Von anderen Autoren 
werden die Angaben, die sich auf die Membrandicke von 1-2 \k 
beziehen, angezweifelt. Von dem Kern der Ent. histolytica schreibt 
Hartmann 1909 : " Im Gegensatz zu E. coli (Schaudinn 1904) und 
E. tetragena (Hartmann 1908) besitzt der Kern keine doppelt kon- 
turierte achromatische Membran^ die bei den beiden anderen Arten 
ziemlich derb ist." 

Awerinzew (Archiv fiir Protistenkunde, 1906, S. 115) unterscheidet 
bei Siisswasserrhizopoden von einer protoplasmatischen Hulle des 
Kernes noch die eigentliche strukturlose Kernmembran, vielleicht ist 
die, protoplasmatische Hulle mit dem " feineren Saum von gleich 
grossen, stark lichtbrechenden Kornchen " zu vergleichen, die nach 
Werner (Handbuch der pathogenen Protozoen, S. 70) die Kernmem- 
bran der Ent. coli zuweilen umgeben. 

Noller konnte bei Ent. aulastomi eine Kernmembran nicht nach- 

(2) Chromatin der Kemsaftzone-Aussenchromatin {Aussenkem). 

Der sogenannte Aussenkem der Entamoben stellt eine Hohlkugel 
dar, in der peripher gegen die Kernmembran iiber ein anscheinend 
meist wabiges Achromatin (Kerngeriist, Linin) Chromatin in Korn- 
chenform von verschiedener Grosse und Miichtigkeit verteilt ist. 
Diese Verhaltnisse sind bei Ent. coli von Schaudinn, Werner, 


Hartmann und Prowazek, bei Ent. tetragena von Viereck, Werner. 
Hartmann u. a., bei Ent. buccalis von Prowazek, Lowenthal, bei 
Ent. williamsi, hartmanni, pithed, polecki von Prowazek, bei Ent. 
aulastomi von Noller, bei Ent. muris sowie einer Amobensp. aus der 
Mans von Wenyon, bei Ent. testvdinis von Hartmann u. a. m. im 
gleichen Sinne beschrieben worden. 

Von der Ent. nipponica schreibt Koidzumi: "The nuclear plasm 
does not show either reticular or alveolar structure. The nucleus is 
very rich in chromatin, which is found condensed into several clumps 
and closely situated on the inner surface of the nuclear membrane." 

Komplizierter ist der Kern der Ent. blattae gebaut; fassen wir die 
von einander etwas differierenden Beschreibungen des Kernaufbaues 
von Schubotz, Elmassian, Mercier und Janicki zusammen, so folgt 
auf die innere Schichte der Kernmembran eine wabig gebaute peri- 
phere Kernzone (a) mit feinem Chromatin, die zentral einen hellen, 
kornchenfreien, wabigen Innenraum (b) einschliesst ; an der Grenze 
zwischen beiden liegen meist kugelig 2-5 \l grosse chromatische " Nu- 
cleolen " (<?). In dem Innenraum ist zuerst von Janicki ein meist 
in Vorbereitung zur Teilung befindliches Karyosom (Netrum nach 
Boveri) nachgewiesen worden (d). 

Der Aussenkern der Entamoben ist von dem Karyosom vielfach 
durch eine helle Kernsaftzone getrennt. 

(3) Karyosom. 

Das Karyosom der Entamoben ist ein wichtiger und notwendiger 
Kernbestandteil, der morphologisch aus Chromatin und Plastin be- 
steht, wobei das erstere Kernelement zunachst in Kornchenform 
reichlich in das Plastin eingetragen ist. Wie weit das Chromatin aus 
Plastin im Sinne von Moroff u. a. entstehen und umgekehrt sich 
wieder zunickverwandeln kann, ist nach dem derzeitigen Stande der 
mikroskopischen Technik Vent Sicherhert nachzuweisen nicht mog- 
lich. Nach Hartmann ist fiir die Existenz eines echten Karyosoms 
der Nachweis eines zentralen Centriols (" Centrosom ") eine Notwen- 
digkeit; fehlt ein Centriol, so muss man die sonst morphologisch 
gleichen Kerngebilde als Pseudokaryosome bezeichnen. Glaser (Ar- 
chiv fiir Protistenkunde, 25. Bd., 1. Heft, 1912) vertritt insofern einen 
anderen Stanclpunkt, als nach ihm das allgemeine Vorhandensein von 
Centriolen im Caryosom aller Protozoen nicht nur nicht bewiesen, 
sondern unwahrscheinlich ist. Als Karyosom definiert er die " Binn- 
enkorper, die bei der Teilung ganz oder zum Teil als Nucleolocentro- 
som wirken." Fiir die Bezeichnung des Karyosoms ware also die 
genaue Kenntnis ihrer Eolle bei der Kernteilung Vorbedingung. Als 
Nukleolocentrosomen oder in einem gewissen Sinne als Netren (Bo- 
veri) teilen sich nun die Binnenkorper bei Ent. buccalis (Prowazek), 
Ent. tetagena (Hartmann) bei Ent. Blattae (Janicki), bei einer 


Amobensp. aus der Maus (Wenyon) vielleicht bei der Ent. muris 
(Wenyon) und Ent. ranarum (Dobell), bei den iibrigen Amoben 
scheint mir der Kernteilungsvorgang noch nicht in diesem Sinne 
genau untersucht worden zu sein und auch bei den oben genannten 
Amoben u verschwindet " auf manchen gerade entscheidenden Stadien 
der Spindelbildung das Karyosom als selbstandiges Kerngebilde, als 
Nukleocentrosoma in der Gesamtspindel und man kann sich von 
seiner von der modernen Zytologie betonten Gesamtkontinuitat nicht 
iiberzeugen. Bei Ent. coli und tetragena scheinen auf der Hohe der 
Spindelentwicklung der Aussenkern und Karyosomkern sich ganz 
durchzumischen und ihre Sonderung aufzugeben, zumal auch die 
Centriolen nicht immer nachweisbar sind. 

Die unvollkommene Kenntnis der Kernteilung kann uns also zu- 
nachst keine Direktiven fur die schwierige Terminologie der einzel- 
nen Kernbestandteile liefern. Kehren wir zu der letzten Definition 
Hartmanns zuriick, so ist ein Centriol bis jetzt sicher nur im Karyo- 
som der Ent. tetragena (Hartmann), Ent. coli (Hartmann), Ent. 
aulastomi (Noller) sowie Ent. testudinis (Hartmann) nachgewiesen 
worden; zeitweise beobachtet ist es bei Ent. muris, Ent. buccalis, Ent. 
polecki sowie Ent. blattae, bei der aber nach Janicki zuweilen sogar 
das ganze Karyosom verschwinden soil. Auch Dobell betont im 
Gegensatz zu Grassi (1881) das Fehlen eines Karyosoms bei Ent. 
ranarum. Glaser meint, dass bei alien Entamoben der kurz vor der 
Teilung gebildete Binnenkorper (Karyosom) iiberhaupt aufgelost 
wird. Bei alien Formen, bei denen die Kontinuitat eines Karyosoms 
durchbrochen ist, wird sich aber de facto eine Kontinuitat eines 
kleinen Kornchens wie es das Centriol ist, kaum nachweisen lassen — 
sie bleibt nur ein theoretisches Desideratum. 

Bei Ent. minuta konnte Elmassian im Karyosom kein Centriol 
nachweisen, bei den iibrigen Amoben sind sonst auch keine Centriolen 
beschrieben worden. 

Aus dieser Zusammenstellung geht hervor, dass sowohl die Defini- 
tion des Karyosoms als des Centriols und die Lehre der Kontinuitat 
leider noch strittig sind und dass nur eine weitere Forschung ohne 
theoretische Voreingenommenheit Klarheit in die verwickelte Sach- 
lage bringen kann. Vorlaufig scheint es aber zweckmassig zu sein, 
das zentrale Plastinchromatingebilde, das im Kern der Entamoben 
zumeist ausgebildet ist, als Karysom zu bezeichnen, ohne sich an 
den Nachweis der Centriolen, der praktisch nicht immer durch- 
fuhrbar ist, zu klammern. 


Im Anschluss an die theoretisch wichtigen Untersuchungen iiber das 
Centrosom von Boveri sowie an die spateren Untersuchungen iiber 
den Blepharoplast und das Karyosom der Flagellaten (1904) wurdeo 


auch am Karyosom periodisch einsetzende Abbauprozesse beobach- 
tet. In dem in einer bestimmten Zeiteinheit fixierten mikrosko 
pischen Bilde stellen sie sich als chromatische Wellen von verschie- 
dener Machtigkeit und variablem Radius dar, die von einem 
Erregungszentrum (Karyosom-Centriol) ausgehen und membran- 
warts fortschreiten. Zyklische Vorgange sind besonders bei Ent. 
tetragena und testudinis von Hartmann beobachtet worden, zeit- 
weise kommen sie auch bei Ent. coli (Werner) vor, ferner sind sie 
bei Ent. polecki geschildert worden. Auch beziiglich dieser zy- 
klischen Prozesse ist die Auffassung der verschiedenen Autoren nicht 
einheitlich, so schreibt H. Glaser (1912) a Es ist zum mindesten ver- 
fruht, im Auf- und Abbau des Karyosoms zyklische Vorgange zu 
sehen, wie sie den Centrosomen der Metazoen eigen sind. Sicher 
ist nur, dass bei den Entamoben der kurz vor der Teilung gebildete 
Binnenkorper wieder aufgelost wird." 


Bis jetzt ist es ungemein schwer, die einzelnen vegetativen Stadien 
der Entamoben von einander zu unterscheiden — da man aber zumeist 
nur vegetative Stadien findet, ware eine solche Unterscheidung auch 
fur die Praxis wichtig, die sich immer wieder mit der Frage, ob 
Ent. coli, histolytica oder tetragena vorliegt, beschiiftigen muss. 
Im Anschluss an die Untersuchungen von Schaudinn hat Hartmann 
sowie F. Craig das Karyosom und seine Struktur der Entamoben bei 
der Differentialdiagnose der Formen beriicksichtigt. 

Nach Hartmann, Whitmore, und Craig ist das Karyosom der Ent. 
coli ahnlich dem der Ent. tetragena, die in ihrem Kernaufbau in 
die Mitte zwischen Ent. histolytica und tetragena zu stellen ist, nur 
spielen sich im Gegensatz zu den Angaben von Werner nicht so 
typische zyklische Prozesse an ihm ab, ferner ist bie Ent. coli in 
20-30 Prozent von alien Individuen das Karyosom immer in Tei- 
lung begriffen. Bei Entamoeba histolytica ist ein kleines Karyosom 
vorhanden (Schaudinn, Hartmann, Craig), das Aussenchromatin 
ordnet sich oft in Klumpen- oder Pigmentform peripher an, die 
doppelt konturierte Kernmembran fehlt und der Kern liegt meist 
excentrisch. Der grosse Wert dieser Diagnose ist aber von verschie- 
denen Autoren angezweifelt worden, so teilweise von H. Werner, 
A. Kuenen u. a. m. 


Ueber das Wesen der Kernteilung der Entamoben konnen wir uns 
zur Zeit keine abschliessende Vorstellung bilden, da bei keiner Amobe 
alle Stadien beobachtet worden sind. Einzelne Kemteilungsbilder 


sind von Ent. tetragena, coli, williamsi, buecalis, minuta, muris, 
ranarum und Ent. blattae beschrieben worden. 

Bei der Kernteilung wird im allgemeinen die Kemmembran nicht 
aufgelost und innerhalb dieser Kernzone spielt sich ein promitoti- 
scher Prozess ab; bei Ent. blattae kommt nach Janicki neben einer 
typischen Amitose auch eine Mitose (Promitose) vor. Bei Ent. 
buccalis teilt sich das Karyosom promitotisch, wahrend der Aussen- 
kern ebenso wie bei einer Amobensp. aus der Maus (Wenyon) durch- 
schniirt wird. Einzelne Kernteilungsbilder der Ent. muris und 
ranarum erinnern gleichfalls an diese Doppelteilung eines Karyo- 
somkernes (Schachtelkernes). Bei Ent. coli, tetragena, williamsi 
u. a. verschwindet auf einigen Stadien die Trennung in Aussenkern 
und Karyosom und es entsteht intranuklear eine Promitose — eine 
primitive Spindel, uber die in Langsreihen angeordnete verschieden 
grosse Chromatinkorner verteilt sind. Beziiglich der weiteren Ein- 
zelheiten muss besonders auf die Abbildungen von Hartmann, We- 
nyon {Ent. muris) und Dobell {Ent. ranarum) verwiesen werden. 

Abweichend verhalt sich die Kernteilung von Ent. blattae. Nach 
Janicki kommt hier eine Amitose mit einfacher Durchschurung der 
einzelnen Kernbestandteile sowie eine Mitose vor. Bei der Mitose 
bildet sich das Karyosom unter Drehung um ca. 90° in eine Zentral- 
spindel um, es treten Chromosomen auf, die die Zahl 6 zu iibertreffen 
scheinen, eine typische achromatische Spindel fehlt, der ubrige 
Kernraum ist mit feinen Kornchen erfullt. In den Telophasen 
knaueln sich die Chrosomen auf. Mercier schildert die Vorgange 
etwas anders, es muss hier diesbeziiglich auf seine Abbildungen ver- 
wiesen werden. Die Kernteilung dauert ca. J Stunde. 


Im Protoplasma einiger Entamoben kommt noch morphologisch 
nicht differ enziertes Chromatin von unregelmassiger Form und 
Anordnung vor, das Schaudinn im Anschluss an E. Hertwig als 
" Chromidium " bezeichnet hatte. Nach den neuesten Forschungen 
ist dessen Funktion und Bedeutung recht zweifelhaft geworden, 
jedenfalls handelt es sich nicht um ein Idiochromidium (Geschlechts- 
chromidium, generatives Chromidium) wie ursprunglich angenom- 
men worden ist. Wahrend der Entwicklung bussen die mor- 
phologisch differenzierten Amobenkerne vielleicht mit Ausnahme der 
Entam. histolytica nicht ihre Umgrenzung ein und zeigen iiberhaupt 
geringe Beziehungen zu den Chromidien, die in der Zyste auftreten. 
Nach Hartmann farben sich die Chromidien bei Ent. tetragena mit 
Karmin, Hematoxylin, Safranin, Methylenblau, Methylgriin und 
weisen weder die Reaktion des Volutin noch des Glykogen auf — "sie 


stammen nich nur aus clem Kern,sondern nehmen im Plasma an Grosse 
unci Zahl enorm zu." Im Laufe der Enzystierung klumpen sie sich zu 
einem Chromidalkorper zusammen. Ihre Bedeutung ist nicht voll- 
kommen klar, " wahrscheinlich handelt es sich um einen Reserve- 
stoff, denn im weiteren Verlauf der Cystenbildung un der sich 
anschliessenden Cystenruhe werden diese Korper in der Regal ganz 
oder fast ganz aufgebraucht." Ueber Chromidien der Ent. coli 
liegen Beobachtungen von Schaudinn, Werner, und Hartmann vor; 
wie bei Ent. williamsi werden die Chromidien in noch jungen 
Cysten unter Stromungserscheinungen nach aussen abgestossen oder 
vererklumpen zu einem grossen Chromidialkorper, der in der Cyste 
" degeneriert." Bei Ent. williamsi^ bei der die Chromidien oft wetz- 
steinformig und fast kristallinisch aussehzen, liegen sie spiiter oft 
kappenformig der fertigen Cyste an. Werner lasst bei Ent. coli auch 
vom peripheren Kernchromatin Chromidien entstehen. Bei Ent. 
hartmanni kommt in der Cyste ein bakteroides, stabchenformig 
gestaltetes Chromidium in Ein- bis Zweizahl vor. Bei Ent. histoly- 
tica riicktnach Schaudinn-Hartmann dasKaryosom an die Kernmem- 
bran heran und gibt chromatisches Material an das Plasma ab, spater 
erfahren die Chromidialbrocken selbsttiitig eine Vermehrung, worauf 
der Kern zusammenschrumpft " entweder ganz aufgelost oder aus 
der Zelle eliminiert " wird. Auf diese Weise entstehen die sog. 
Chromiclialtiere (Hartmann) (vergl. Ent. buccalis) ; ahnlich wie 
Schaudinn liefert Craig (1908) eine Schilderung der Chromidien- 
Cystenbildung der Ent. histolytica (vergl. noc. 1909). Chromidien 
hat ferner W. Noller bei Ent. aulastromi beschrieben. 


Yon fast alien Autoren, die sich mit der Untersuchung der Biologie 
der Entamoben beschaftigt haben, sind Kerndegenerationen be- 
schrieben worclen, die einen sehr mannigfachen Verlauf nehmen 
konnen, beziiglich der Einzelheiten muss auf die speziellen Arbeiten 
verwiessen werden. Die Kerndegeneration der Ent. ranarum hat 
Dobell zum Gegenstand einer besonderen Studie gemacht und sie mit 
der Depressionslehre Hertwigs in Zusammenhang gebracht. Bei Ent. 
tetragena unterscheidet Hartmann zwei Haupttypen von Degenera- 
tionsformen (a) Formen. bei denen sich das Chromatin in Form von 
grosseren Brocken an der Kernmembran ansammelt, (b) Formen- 
reihen, bei denen die Kernmembran schwindet und nur noch ein 
grosses Karyosom iibrig bleibt. 

Ueber Kerndegenerationen bei Ent. williamsi hat Prowazek, bei 
Ent. aulastomi W. Noller berichtet, ferner sind diesbeziigliche Anga- 
ben in den Arbeiten von Casagrandi-Barbagallo sowie Noc zu finden. 
CGG92— vol 2, pt 1—13 13 



By Albert Hassall, Assistant Zoologist, United States Department of Agri 

culture, Washington, D. C. 

Apis mellifica : 

apis Fantham & Porter: Entamoeba. 


aiClastomi Noeller : Entamoeba. 
Bee. See Apis mellifica. 
Blatta orientalis : 

Mattae Buetschli : Amoeba, Endamoeba. 

Olattarum Calandruccio : Amoeba. 

sp. : Amoeba. 
Bombinator" pachypus : 

currens Metcalf: Amoeba (Entamoeba). 


bovis Liebetanz : Amoeba. 
coli Loesch : Amoeba. 
oblonga Celli & Fiocca : Amoeba. 
Box boops : 

sp. Ckatton : Amoeba. 


currens Metcalf: Amoeba (Entamoeba). 


ranarum (Grassi) : Entamoeba. 
Canis familiaris : 

coli Loesch: Amoeba, Endamoeba, Entamoeba 

fecalis Walker : Ameba. 

phagocytoides Ganducheau : Entamoeba. 
Cat. See Felis domestica. 
Cavia cobaya: 

cobayae Walker: Ameba. 

coli Loesch : Amoeba. 

fecalis Walker: Ameba. 

spinosa Celli & Fiocca : Amoeba. 
Chieonomus sp. (larva) : 

chironomi Porter: Amoeba. 


croupogena Rivolta & Delprato : Amdba. 
Dog. See Canis familiaris. 
Eideciise. See Lacerta. 
Equus caballus : 

coli Loesch: Amoeba. 

feoalia Walker: Ameba. 

inte8tinali8 Walker: Ameba. 

letullei Neveu-Lemaire : Amoeba. 

coli Loesch : Amoeba. 

coli fells Quincke & Roos: Amoeba. 

coli mitis Quincke & Roos: Amoeba. 


Felts domestica — Continued. 

entcrica Walker: Ameba. 

fecalis Walker: Ameba. 

intestinalis Walker : Ameba. 

intestini vulgaris Quincke & Roos: Amoeba. 

Umax Williams & Gurley: Amoeba. 

tetragena Viereck: Entamoeba. 
Flies : 

Umax Werner : Amoeba. 
Frogs : 

spinosa Celli & Fiocca : Amoeba. 
Guinea pig. See Cavia cobaya. 
Homo sapiens : 

africana Hartmann : Entamoeba. 

buccalis Steinberg: Ameba, Entamoeba. 

buetschlii von Prowazek : Entamoeba. 

cochinchinensis Sluiter & Swellengrebel : Entamoeba. 

coli Loesch : Ameba, Entamoeba. 

coli fells Quincke & Roos: Ameba. 

coli mitis Quincke & Roos: Ameba. 

dentalis Braun : Ameba. 

diaphana Celli & Fiocca : Ameba. 

dysenteriac Councilman & Lafleur : Amoeba. 
' dysentcrica Pfeiffer : Amoeba. 

febris flavae Thayer : Amoeba. 

febris tertianac Kruse : Amoeba. 

foliata Casagrandi & Barbagallo : Amoeba. 

gingivalis Gros : Ameba. 

guttula Celli & Fiocca : Amoeba. 

kartmanni von Prowazek : Entamoeba. 

histolytica Schaudinn : Entamoeba. 

hominis Casagrandi & Barbagallo : Entamoeba. 

hominis Craig: Paramoeba. 

hominis Walker : Ameba. 

incapsulata Wesener : Amoeba. 

intestinalis Blancbard : Amoeba. 

intcstini vulgaris Quincke & Roos: Amoeba. 

jelaginia von Merescbkowsky : Amoeba. 

kartiilisi Doflein : Ameba. 

letullei Neveu-Lemaire : Amoeba. 

lobosa Celli & Fiocca : Ameba. 

lobosa var. coli Celli & Fiocca : Ameba. 

lobosa gruberi Wuelker : Amoeba. 

lobosa guttula Celli & Fiocca : Ameba. 

lobosa oblonga Celli & Fiocca : Ameba. 

lobosplnosa Craig : Ameba. 

malariae Laveran : Amoeba. 

malariac febris quartanae Kruse: Amoeba. 

minuta Elmassian : Amoeba, Entamoeba. 

miurai Ijima : Ameba, Eudamoeba. 

mortinatalium Smith & Weidman: Amoeba, Entamoeba. 

nipponica Koidzumi : Amoeba, Entamoeba. 

phagocytoidcs Gauducheau : Amoeba, Entamoeba. 


Homo sapiens — Continued. 

polecki von Prowazek : Entamoeba. 

pulmonalis Artault: Amoeba. 

reticularis Celli & Fiocca : Ameba. 
sp. Fantham: Entamoeba. 

spinosa Celli & Fiocca : Ameba. 
tetragena Viereck : Amoeba, Entamoeba. 

tropicalis Lesage : Amoeba, Entamoeba. 

undulans Celli & Fiocca : Amoeba. 

undulans Castellani : Entamoeba. 

urogcnitalis Baelz : Ameba. 

vaginalis Blanchard : Amoeba. 

vermicularis Celli & Fiocca : Ameba. 

viridis Wuelker: Amoeba. 

vulgaris Roos : Amoeba. 

williamsi von Prowazek: Entamoeba. 
Horse. See Equus caoallus. 
House mouse. See Mus musculus. 
Laceeta : 

lacertae Hartmann : Amoeba. 
Lacerta agilis : 

lacertae Hartmann : Amoeba. 
Lagopus scoticus : 

lagopodis Fantham: Amoeba (Entamoeba). 

sp. Shipley : Amoeba. 
Lepus cuniculus. [See also Rabbit.] 

enierica Walker : Amoeba. 
Limax : 

Umax Pfeiffer: Amoeba. 
Lymnodynastes tasmaniensis : 

morula Raff: Entamoeba. 
Macacus cynomolgus : 

sp. Musgrave & Clegg: Amoeba. 
Macacus philippinensis : 

sp. Musgrave & Clegg: Amoeba. 
Macacus pileatus : 

nuttalli Castellani : Entamoeba. 
Macacus sinicus : 

sp. Chatton : Loeschia. 
Meleagris gallopavo : 

enierica Walker: Ameba. 

gallopavonis Walker: Ameba. 

intestinalis Walker : Ameba. 

melcagridis Smith : Amoeba. 
Molge palmata : 

ranarum (Grassi) : Entamoeba. 
Monkey : 

lobospinosa Craig: Ameba. 

sp. Fantham: Entamoeba. 

tetragena Viereck : Entamoeba. 


enierica Walker: Ameba. 
spinosa Celli & Fiocca : Amoeba. 


Mrs musculus : 

ent erica Walker: Ameba. 

fecaUs Walker: Ameba. 

muris Grassi : Amoeba, Entamoeba. 

musculi Walker: Ameba. 
Mus rattus : 

muris Grassi : Amoeba. 

"Amibes" Stiles & Hassall. 
Mus spp. : 

muris Grassi : Amoeba. 


testudinis Hartmann : Entamoeba. 
Ovis aries : 

parasitica Lendenfeld : Amoeba. 

sp. Blanc : Amoeba. 
Peltogaster curvatus : I 

pacdophthora Caullery : Amoeba. 
Peri planet a orientalis : 

blattae Buetschli : Amoeba, Entamoeba. 
Pig. See Sus scrofa. 
Pigeon. See Columba domestica. 


pithed von Prowazek : Entamoeba. 
Rabbit. [See also Lepus cunicuhis.'] 

fecalis Walker : Ameba. 
Rana esculenta : 

currens Metcalf: Amoeba (Entamoeba). 

ranarum Grassi : Amoeba, Entamoeba. 

spinosa Celli & Fiocca : Amoeba. 
Rana sp. : 

ranae Walker: Ameba. 

rotatoria Mayer: Amoeba. 
Rana temporaria : 

ranarum (Grassi) : Entamoeba. 
Rat. See Mus decumanus. 
Red grouse. See Lagopus scoticus. 
Sag itt a claparedei : 

chaetognathi Grassi : Amoeba. 

pigmentifcra Grassi : Amoeba. 

sagittae Grassi : Amoeba. 
Sheep. See Ovis aries. 
Spadella bipunctata : 

chaetognathi Grassi: Amoeba. 

pigmentifera Grassi : Amoeba. 

sagittae Grassi : Amoeba. 
Spadella inflata : 

chaetognathi Grassi : Amoeba. 

pigmentifera Grassi : Amoeba. 

sagittae Grassi : Amoeba. 
Spadella serratodentata : 

chaetognathi Grassi: Amoeba. 

pigmentifera Grassi : Amoeba. 

sagittae Grassi : Amoeba. 


Stylopyga orientalis : 

blattae (Buetschli) : Entamoeba. 


succinea Pfeiffer : Amoeba. 
Sus scrofa : 

fecalis Walker : Ameba. 

intcstinalis Walker : Ameba. 

polecki von Prowazek : Entamoeba. 

spinosa- Celli & Fiocca : Amoeba. 
Symphodus melops : 

mucicola Cbatton : Amoeba. 
Symphodus tinca : 

mucicola Chatton : Amoeba. 
Testudo graeca : 

testudinis Hartmann : Entamoeba. 
Turkey. See Mcleagri^ gallopavo. 
White mouse: 

fecalis Walker: Ameba. 


By Albert Hassall, Assistant Zoologist, United States Department of Agri- 
culture, Washington, D. C. 

Abbott, Alexander C. [Prof., Hyg., Univ. Penn.] 

1899. — The hygiene of transmissible diseases; their causation, modes of 
dissemination, and methods of prevention. 311 pp., 44 figs. 8°. Phila- 
delphia. [Wm.] 
Achard, H. J. [M. D., Chicago, 111.] 

1911. — The copper salts and ipecacuanha in the treatment of amebic 
colitis <Charlotte [N. C] M. J., v. 64 (3), Sept., pp. 179-181. [Wm.] 
Adams, S. S. [Dr.] 

1907.— [Discussion of Lamb, D. S., 1907, pp. 354-356] <Wash. M. Ann. 
(1907-03), v. 6 (5), Nov., p. 356. [Win.] 
A.dier. [Dr.] 

1900. — [Amoebic dysentery.] [Abstract of remarks before N. York Acad. 
Med., Feb. 20] <Med. News, N. Y. (1418), v. 76 (11), Mar. 17, p. 434. 
[Wa, Wm.] 
Akashi, M. 

(1911). — Ueber die Morphologie und Entwicklung der Darmamoben. 

[Japanese text] <Mitt. d. med. Gesellsch. zu Tokio, v. 25 (6). 
1911. — Idem. [Abstract by Fukuhara] <Centralbl. f. Bakteriol. [etc.], 
Jena, 1. Abt, v. 50 (19-21), 4. Dec, Ret, pp. 659-660. [Wa, Wm.] 
Albu, A. [Dr., Berlin.] 

1905. — Demonstration der anatomischen Priiparate eines Falles von ein- 
heimischer Amoben-Dysenterie. [Read before Ver. f. inn. Med., Berl., 
12. Dec. 1904] < Deutsche med. Wchnschr., Leipz., v. 31 (1), 5. Jan., 
pp. 43^14; discussion, p. 44. [Wa, Wm.] 
1905.— Zur Kenntniss der sporadischen einheimischen Dysenterie <Ztschr. 
f. klin. Med., Berl., v. 56 (5-6), pp. 432^48, figs. 1-4. [Wm.] 
Albu, A. ; & Werzberg, A. 

1912. — Beitriige zur Kenutnis der Amoebendysenterie und enterogenen 
Eosinophilic <Ztschr. f. klin. Med., Berl., v. 74 (5-6), pp. 394-403, 1 fig. 
[Wm. | 


Alexeieff, A. 

1912. — Sur le stade flagelle dans Involution des amlbea Umax. 1. Stade 

flagelle chez Amoeba punctata Dangcard <Compt. rend. Soc. de biol., 

Par., v. 72 (4), 2 few, pp. 126-128. [Wa, Wn:, Wc] 
1912. — Sur les caracteres cytologiques et la sy sterna tique des amibes du 

groupe Limax (Nacglcria nov. gen. et HartmcmrUa hot. gen.) et des 

arnibes parasites des vertebres (Proctamocba nov. gen.) <Bull. Soc. 

zool. de France, Par., v. 37 (2), 5 avril, pp. 55-74, figs. 1-7. [Wa.] 
1912. — Quelques remarques complementaires sur la sysh'matique des 

amibes du groupe Limax <Ibidem (4), 4 juin, pp. 149-157, fig. 1. [Wa.] 
1912. — Sur quelques protistes parasites intestinaux d'une tortue de Ceylan 

(Nicoria trijuga) <Zool, Anz., Leipz., v. 40 (4-5), 30 Aug., pp. 97-105, 

figs. 1-3. [Wa.] 
Allan, William. [A. B., M. D. ; Prof., Parasitol., North Carolina Med. Coll., 

Charlotte, N. C] 
1909. — Amoebic dysentery with abscess of liver — confirmed at autopsy 

< Charlotte [N. C] M. J., v. 60 (3), Sept., pp. 144-145. [Wm.] 
1909. — Intestinal parasites and the diagnosis of neurasthenia < South. 

M. J., Nashville, v. 2 (10), Oct., pp. 1037-1038. [Wm.] 
1909. — A small localized epidemic of amebiasis <J. Am. M. Ass., Chicago, 

v. 53 (19), Nov. 6, pp. 1561-1562. [Wa, Wm, Wc] 
1909.— Amoebae in the stools of pellagrins <N. York M. J. [etc.] (1620), 

v. 90 (25), Dec. IS. pp. 1212-1213. [Wa, Wm, Wc] 
1910.— Contact infection in amebiasis <Med. Rec, N. Y. (2044), v. 77 (2), 

Jan. 8, p. 63. [Wa, Wm, Wc] 
1910.— Eosinophilia in amoebiasis <Med. Era, St. Louis, v. 19 (3), Mar., 

p. 109. [Wm.] 
1910. — Studies in amebiasis, with a report of forty-two cases. [Read before 

12. Ann. Sess. Tri-State Med. Ass. Carolinas & Virginia, Richmond, Feb. 

15-17] <Med. Rec, N. Y. (2068), v. 77 (26), June 25, pp. 1092-1093. 

[Wa, Wm, Wc.] 
1910. — Studies in amediasis, with a report of forty-two cases < Charlotte 

[N. C] M. J., v. 62 (3), Sept., pp. 181-183. [Wm.] 
1911.— The amebic dysentery problem in North Carolina <Ibidem, v. 63 

(2), Feb., pp. 87-89. [Wm.] 

Amberg, Samuel. 

1901. — A contribution to the study of amoebic dysentery in children. [Read 
Jan. 7] < Johns Hopkins Hosp. Bull., Bait. (129), v. 12, Dec, pp. 355-363. 
[Wa, Wm.] 
Anders, James M. [M. D., LL.D.] ; & Rodman, William L. [M. D., LL.D.]. 

1910. — The treatment of amebic dysentery, especially by appendicostomy. 
[Read before 16. Interna t. Med. Cong., Aug. 29-Sept. 4, 1909] <J. Am. 
M. Ass., Chicago, v. 54 (7), Feb. 12, pp. 503-506. [Wa, Wm, Wc] 

Anderson, A. R. S. 

1907. — Note on the occurrence of Amoeba coli in Port Blair, Andaman 
Islands <Indian M. Gaz., Calcutta, v. 42 (4), Apr., pp. 126-12S. [Wm.] 

1908. — Dysentery with intestinal amoebae, but without hepatic abscess. 
[Read before 76. Ann. Meet. Brit. Med. Ass., Sheffield, July] <Brit 
M. J., Lond. (2495), v. 2, Oct 24, pp. 1243-1244. [Wa, Wm.] 

Andresen, Albert F. R. [M. D.] 

1911.— Amebic dysentery <Med. Rec, N. Y. (2141), v. 80 (21), Nov. 13, 
pp. 1024-1026. [Wa, Wm.] 


Artault, Stephen. 

1898. — Flore et faune des cavernes pulmonaires <Arch. de parasitol., 
Par., v. 1 (2), avril, pp. 217-307, pi. 1, figs. 1-6, 1 chart. [Wa.] 
Ascher. [Dr., k. Stadtwundarzt] 

1899.— Studien zur Aetiologie der Ruhr und zur Darmflora <Deutsche 
med. Wchnschr., Leipz., v. 25 (4), 26. Jan., pp. 56-57. [Wa, Wm.] 
Ascoli, Maurizio. [Prof.] 

1912. — Dissenteria da Entameha tetragena in soldato reduce da Tobruk. 
[Read before Accad. Gioenia di sc. nat. in Catania, 9 mar.] <Riforina 
med., Napoli, v. 28 (15), 13 apr., pp. 393-394. [Wm.] 
Ashburn, Percy M. ; & Craig, Charles F. [Asst. Surgs., U. S. Army.] 

1907. — The work of the Army Board for the study of tropical diseases in 
the Philippine Islands <Mil. Surg., Carlisle, Pa., v. 21 (1), July, pp. 
38-49, 7 figs.; (2), Aug., pp. 140-148; (3), Sept., pp. 220-225; (4), Oct., 
pp. 336-348; (6), Dec, pp. 527-530. [Wm.] 
Asman, Bernard. 

1910— [Discussion of Hanes, Granville S., 1910, pp. 1639-1641] Ken- 
tucky M. J., Bowling Green, v. 8 (10), June 15, p. 1641. [Wm.] 
Aubry, P. [Prof, suppl., m€d. d. hop.] 

1907. — Dysenterie bacillaire et dysenterie amibienne; quelqnes notions 
recentes <Gaz. m€d. de Nantes, v. 25 (24), 15 juin, pp. 461-467. [Wm.] 
Auche, B. ; & Campana (Mile.). 

1905. — Note sur la dysenterie chez les enfants a Bordeaux. [Remarks 
before Soc. de med. et de chir. de Bordeaux, 3 fev.] <Gaz. hebd. d. sc. 
med. de Bordeaux, v. 26 (10), 5 mars, pp. 117-118. [Wm.] 
Aurand, W. H. [Dr.] 

1905. — Amebic dysentery <Northwest. Lancet, Minneapolis, v. 25 (17), 
Sept. 1, p. 321. [Wm.] 
Austin, H. W. [Surg., U. S. Public Health & Mar.-Hosp. Serv.] 

1909. — Amoebic dysentery in San Francisco, Cal. <Pub. Health Rep., 
U. S. Mar.-Hosp. Serv., Wash., v. 24, pt. 2 (39), Sept. 24, pp. 1404-1405. 
[Wa, Wm.] 
Awerinzew, S. 

1909. — Studien iiber parasitische Protozoen. 1. Die Sporenbildung bei 
Ceratomy.ra drepanopsettae mihi <Arch. f. Protistenk., Jena, v. 14 (1), 
pp. 74-112, pis. 7-8. [Wa, Wm.] 
Axisa. Edgar. [Primiirarzt, Dr.] 

1910. — Die Behandlung der Amoben-Dysenterie <Therap. d. Gegenw., Berl. 

& Wien, 51. J., n. F., v. 12, Juni, pp. 263-270. [Wm.] 
1910. — Die Amoben-Dysenterie <Arch. f. Verdauungskr., Berl., v. 16 (6), 
15. Dec, pp. 667-699. [Wm.] 
Axtell, W. H. [M. D., Bellingham, Wash.] 

1911. — Amebic dysentery contracted in the Arctics of Alaska. Report of a 
case <Northwest Med., Seattle, Wash., v. 3 (2), Feb., pp. 51-52, figs, 
a-d. [Wm.] 
Babes, Victor; & Zigura, Y. 

1894. — Etude sur l'entero-hepatite suppuree endemique <Arch. de med. 
expSr. et d'anat. path., Par., 1. s., v. 6 (6), l or nov., pp. 862-882, pis. 
15-16, figs. 1-6. [Wa, Wm.] 
(1895). — Etude sur l'entero-hepatite suppuree endemique <Ann. de 1'Inst. 
de path, et de bacteriol. de Bucarest, pp. 211-255. 
Raelz, B[rwln]. [Prof., Tokyo, Japan.] 

1883 a. — Ueber elnige neue Paraslten des Menschen <Berl. klin. Wchnschr., 
v. 20 (16), 16. Apr., pp. 234-238, figs. 1-3. [Wa, Wm.] 


Balfour, Andrew. 

1911. — Miscellaneous notes <4. Rep. Wellcome Trop. Research Lab. [etc.], 
Lond., v. A, Med., pp. 362-36S, figs. 109-117, pi. 22, fig. 1: pi. 23, figs. 

1-4. [Wm.] 
Ball, A. Brayton. [M. D., Visit. Physician, N. York Hosp. & St. Luke's Hosp.] 
1892. — The symptoms, complications, and treatment of dysentery <Therap. 
Gaz., Detroit, Mich., & Phlla., Pa., v. 16, 3. s., v. 8 (7), July 15, pp. 
442^48; (8), Aug. 15, pp. 518-526. [Win.] 
Barbagallo, Pietro. [Dr.] 

1905. — V Entamoeba Jiominis (Casagrandi e Barbagallo, 1897) e V Enta- 
moeba histolytica (Schaudinn, 1903) in rapporto con la cosidetta dissen- 
teria amebica <Rassegna internaz. d. med. mod., Catania, v. 6 (10), 31 
magglo, pp. 73-75. [Win.] 
1905.— Idem <Policlin., Roma, v. 12 (6), giugno, pp. 282-288. [Wm.] 
1905. — Sulla pretesa coltivazione delle amebe parassite <Rassegna in- 
ternaz. d. med. mod., Catania, v. 6 (19), 15 ott, pp. 145-146. [Wm.] 
1906. — Idem <Gazz. d. osp., Milano, v. 27, 1. semestre (36), 2 mar., pp. 
380-381. [Wm.] 
Barr, Richard A. [Dr.. Nashville, Tenn.] 

1909. — [Discussion of Bates, John Pel ham, 1909, pp. 56-59] <J. Tennessee 
State M. Ass., Nashville, v. 2 (2), June, pp. 62; 63; 64-65. [Wm.] 
Bartley. Elias H. [M. D. ; Prof., Chem. & Toxicol., Long Island Coll. Hosp.] 
1898.— The feces [Amcba coli] <Text-book Med. & Pharm. Chem. (Bartley), 
Phila., 5. ed., pp. 606-610. [Wm.] 
Basseres, F. [Med.-maj. de l re cl. & l'h6p. mil., Perpignan.] 

1911. — Abc&s amibien du foie et phagedenisme cutane amibien post- 
operatoire; association staphylococcique secondaire <Arch. de med. et 
de pharm. mil., Par., v. 57 (4), avril, pp. 256-272, figs. 1-2. [Wm.] 
Bassett-Smith, P. W. [Staff-Surgeon, R. N.] 

1900 a. — Abscess of the left lobe of the liver, with particular reference to 
its amoebic causation <Brit. M. J., Lond. (2070). v. 2, Sept. 1, pp. 
552-553. [Wa, Wm.] 

1901 a.— Idem <J. Trop. M., Lond., v. 4 [ (2) ]. Jan. 15, pp. 33-34. [Wm.] 
Bates, John Pelham. [M. D. ; Lecturer, Trop. Dis., Med. Dept, Vanderbilt 

Univ., Nashville, Tenn.] 
1909. — Amebic dysentery and appendicostomy. [Author's abstract of pape: 

read before 26. Ann. Meet. Tennessee State Med. Ass., Nashville, Apr. 

13-15] <J. Am. M. Ass., Chicago, v. 52 (18), May 1, pp. 1449-1450; dis- 
cussion, p. 1450 [Wa, Wm, We.] 
1909. — Amebic dysentery and appendicostomy <J. Tennessee State M. Ass.. 

Nashville, v. 2 (2), June, pp. 56-59; discussion, pp. 60-65. [Wm.] 
de Beaurepaire Aragao, LI. [Dr.] 

1909. — Sobre a Amoeba diplomitotica n. sp. Contribuigao para o estudo da 

divizao nuclear nas amebas <Mem. Inst. Oswaldo Cruz. Rio de Ja- 

neiro-Manguinhos, v. 1 (1), abril, pp. 33-43, pi. 2, figs. 1-22. [Wa.] 
(1912). — [Entamoeba brasiliensis] <Brazil med., Rio de Jan., v. 26 (7), 

15 feb. 
Behla, Robert. [Sanitatsrath.] 

1S98 b. — Die Amoben insbesondere vom parasitiiren und culturellen Stand- 

punkt. vi+73 pp., 1 pi. 8°. Berlin. [Pa ba .] 
Beijerinck, M. W. [Delft] 

1896 a. — Kulturversuche mit Amoben auf festem Substrate <Centralbl. f. 

Bakteriol. [etc.], Jena, 1. Abt, v. 19 (8), 28. Feb., pp. 257-267, pi. 7, figs.- 

1-12. [MS. dated 25. Dec. 1895.] [Wa, Wm.] 


Beijerinck, M. W. — Continued. 

1S97 a. — Amobenkultur auf festen Substraten. Antwort an Herrn Celli. 
[See Celli, Angelo; & Fiocca, R., 1895 a] <Ibidem, v. 21 (3), 30. Jan., 
pp. 101-102. [MS. dated 6. Jan.] [Wa.] 

Bell, John. [L. R. C. P. Lond. ; M. R. C. S. Eng. ; Supt, Govt. Civil Hosp., 
Hong Kong.] 
1909. — A new parasite seen in a case of dysentery <Lancet, Lond. (4455), 
v. 176, v. 1 (3). Jan. 16, p. 161, figs. 1-4. [Wa, Win.] 
Bensen, W. [Dr., Marinestabsarzt] 

1908. — Die Darinprotozoen des Menschen. [Read before Naturf. Versaminl. 
zu Koln] <Arch. f. Schiffs- u. Tropen-Hyg., Leipz., v. 12 (20), Oct., 
pp. 661-676, figs. 1-7. [Win.] 

Benidt, Fritz [? Frieclrich Wilhelm August]. [Dr., Stralsund.] 

19,04 a. — Protozoen in einem Leberabscess. [Read before Aerztever. d. 
Reg.-Bezirks Stralsund, 12. Nov. 1893] < Deutsche Ztsehr. f. Chir., 
Leipz., v. 40 (1-2), 20. Dec., pp. 163-172, figs. 1-2. [Wm.] 
Berry, T. D. [Dr.] 

1903.— [Discussion of Young, G. B., 1903, pp. 241-248] <Ain. Pract. & 
News, Louisville, v. 35 (7-S), Apr. 1 & 15, pp. 290-291. [Wm.] 
Bertarelli, E. [Asst, 1st. d'Ig., r. Univ., Torino.] 

1905. — Le amebe e la dissenteria amebica <Riv. d'ig. e san. pubb., 

Torino, v. 16 (7), 1° apr., pp. 193-198. [Wm.] 
1905. — Die Ainoben und die Amobenrulir <Wien. klin. Rundschau, v. 19 

(23), 11. Juni, pp. 397-399. [Win.] 
1912. — Amebe ed amebiosi umane alia luce delle moderne conoscenze 
<Gazz. d. osp., Milano, v. 33 (6), 14 gennaio, pp. 49-51. [Wm.] 


1911.— [Note to Manaud, A., 1911, pp. 322-325] <Bull. Soc. de path, exot, 
Par., v. 4 (5), 10 mai, p. 325. [Wa, Wm.] 

Beyerinck, M. W. See Beijerinck, M. W. 
Billet, A. [Med.-maj. de l re classe.] 

1905. — Eosinophilic dans la dysenterie amibienne. [Read 16 mai] <Compt. 

rend. Soc. de biol., Par., an. 57, v. 58 (19), 2 juin, pp. 874-876. [Wa, 

Wm, Wa] 
1907. — Sur un cas de dysenterie nostras a amibes. [Read 13 juin] <Ibidem, 

an. 59, v. 62, v. 1 (23), 5 juillet, pp. 1232-1234. [Wa, Wm, Wa] 
1907. — Sur un cas de dysenterie " nostras " a amibes <Caducee, Par., v. 

7 (14), 20 juillet, p. 190. [Wm.] 
1907. — De la dysenterie & Trichomonas <Ibidem (16), 17 aout, pp. 215- 

217, figs. 1-6. [Wm.] 
Bizzozero, Giulio. [Dr., Prof, ord., patol., r. Univ. di Torino.] 

1882 a. — Manuale di microscopia clinica, con aggiunte risguardanti gli 

esami chimici piu utili al practico e l'uso del microscopio nella medicina 

legale. 2. ed. completamente rifusa ed aumentata. xii+246 pp., 39 figs., 

7 pis., 80 figs. 8°. Milano. [Wm.] 
1883. — Handbuch der klinischen Mikroskopie. Mit Beriicksichtigung der 

wichtigsten chemischen Untersuchungen am Krankenbette und der 

Verwendung des Mikroskopes in der gerichtlichen Medicin. Autorisirte 

deutsche Original-Ausgabe besorgt von Alexander Lustig und Stefan 

Bernheimer. Mit einem Vorwort von Hermann Nothnagel. xii+251 pp., 

39 figs., 7 pis., 80 figs. 8°. Erlangen. [Wm.] 


Bizzozero, Giullo — Continued. 

1887. — Idem. Mit Beriicksiclit igung der Verwendung des Mikroskopfl in der 
gerichtlichen Medizln. 2. vermehrte und verbesserte Aufl. der deutschen 
Original-Ausgabe besorgt von Stefan Bernhelmer. .Mit einem Vorw 
von Hermann Nothnagel. viii+352 pp., 40 figs., 8 pis., 100 figs. 8°. 
Erlangen. [Win.] 

Blackham, R. J. [Major, Roy. Army Med. Corps; D. P. H.] 

1906.— Tropical dysentery <Lancet, Lond. (4344), v. 171, v. 2 (22), Dec. 1, 

pp. 3493-1500, 1 chart, 1 table. [Wa, Win.] 
1908. — The treatment of dysentery. [Read before Douglas Cong., July, 

1907] <J. Roy. Inst. Pub. Health, Lond., v. 16 (2), Feb., pp. 77-88, 1 

chart. [Wa.] 
Blanc, Antoine-Frangois-Louis. [Chef, trav. d'histol., Ecole vet., Lyon.] 

1S98 a. — Sur une amibe vivant accidentellement dans le poumon du mouton 

<J. de med. vet. et zootech., Lyon, v. 49, 5. s., v. 2, sept., pp. 513-515. 

1899 c— Idem [?] <Ann. Soc. Linn, de Lyon (1898), n. s., v. 45, pp. 87-89. 

Blanchard, Raphael Anatole Einile. [Prof., Ecole de med., Paris.] 

1885 g. — Traite d6 zoologie medicale. v. 1 : Protozoaires, histoire de l'oeuf, 

coelenteres, echinodermes, vers (aneuriens, plathelminthes, nemathel- 

minthes). Fa se. 1, pp. 1-192, figs. 1-124. 8°. Paris. [Published Nov. 4.] 

[Wa, Wm.] 
[18S8 1].— Amibe <Grande encycl., Par., v. 2, pp. 740-741, figs. 1-7. [Wc] 
1S90 b. — Los animales parasitos introducidos por el agua en el organismo. 

132 pp., 50 figs. 8°. Londres. [Reprinted from Blanchard; Salzar; & 

Newman, C. Examen quimico y bacteriologico de las aguas potables. 

Chile.] [Lib. Stiles.] 
1890 c. — Les animaux parasites introduits par l'eau dans l'organisme, 

[Transl. of 1S90 b, by author] <Rev. d'hyg., Par., v. 12 (9), 20 sept., 

pp. 828-870, figs. 1-27, 2 tables; (10), 20 oct, pp. 923-969, figs. 28^7, 2 

tables. [Wm.] 
1890 d.— Idem <Bull. Soc. de med. pub., Par., v. 13, pp. 23S-326, figs. 1-47, 

tables. [Wm.] 
1896 b. — Parasites animaux <Traite de path. gen. (Bouchard), Par., v. 2, 

pp. 649-810, figs. 47-109, 1 table. [Wm.] [A reprint of this was re- 
ceived by Dr. Stiles in 1S95. The title-page of v. 2, however, bears date 

of 1896.] 
1904. — Zoologie et medecine. [Read before 6. Cong, internat. de zool., 

Berne, 15 aout] <Arch. de parasitol., Par., v. 9 (1), l er dec, pp. 129-144. 

[Wa, Wm.] 

Blumer, George. 

1903.— Report on Dr. R. W. A.'s stools [see Ward, Samuel B., 1903 a] 
< Albany M. Ann., v. 24 (1), Jan., p. 26. [Wm.] 

1896 a. — Ueber Amobenenteritis. [Presented before Ver. f. inn. Med.] 
<Deutsche med. Wchnschr., Leipz. & Berl., v. 22 (14), 2. Apr., pp. 
214-217, figs. 1-^. [Wa, Wm.] 
Boas, J[ohan] E[rik] V[esti]. [Dr., Prof., Zool., k. landwirtschaftl. Hoch- 
schule, Kopenhagen.] 
1911, — Lehrbuch der Zoologie fur Studierende. 6. vermehrte und verbes- 
serte Auflage. x-f-690 pp., 618 figs. 8°. Jena. [Wa.] 


Boese. [Dr., Marine-Oberstabsarzt.] 

1908. — Beobacbtungen und Erfabrungen uber Rubr in Ostasien. <Ztschr. f. 
Hyg. u. Infektionskr., Leipz., v. 61 (1), 3. Sept., pp. 1^8, pis. 1-8. 
[Wa, Win.] 
Boggs, Thomas R. [M. D., Baltimore, Md.] 

190S. — Amoebic dysentery in tbe soutbern states. [Read before Meet. Tri- 
State Med. Ass., Cbarlotte, N. C, Feb. 18] <Virginia M. Semi-Month., 
Ricbmond (289), v. 13 (1), Apr. 10, pp. 9-12. [Wa, Wm.] 
Boinet, E. 

1909. — Abces dn foie dysenterique nostras. [Read 29 juin] <Bull. Acad, 
de med., Par., an 73, 3. s, v. 61 (26), pp. 705-719. [Wm.] 
de Bonis, Teodosio. [Prof, agreg. patol. gen., Univ. Napoli.] 

1882 a. — Los parasitos del cuerpo bumano en relacion con las alteraciones 
locales y generales del organismo. Traducida del italiano y considerable- 
mente aumentada con notas y nn vocabulario de parasitologia por Carlos 
Maria Cortezo. xiii+311 pp., 22 figs., pi. 1, 13 figs.; pi. 2, 18 figs. 8°. 
Madrid. [Wm.] 
Booth, R. T. [M. B., B. Cb., D. T. M. H„ Hankow.] 

1908. — Investigation of tbe cause of dysentery. [Read before C. C. M. 
Ass., Hankow, Apr. 15] <Cbina M. J., Shanghai, v. 22 (6), Nov., pp. 
339-353. [Wm.] 

1896 a. — De l'enterite amibienne <Semaine med., Par., v. 16 (11), 26 few, 
p. 87. [Wm.] 
Borini, Agostino. [Dr., r. Univ. di Torino.] 

[1904]. — I protozoi parassiti dell' intestino umano in rapporto alia diag- 
nostica clinica. Con prefazione del E. Perroncito. 40 + [1] pp., 11 figs. 
24°. Torino. [Wm.] 
Bory de Saint-Vincent, Jean-Baptiste George Marie Marcellin (Baron). 

1822 a.— Amibe. Amiba <Dict. class, d'hist. nat., Par., v. 1, pp. 260-262. 
Bose, Kailas Ch. [Calcutta.] 

1908. — Is dysentery the sole cause of the tropical liver abscess? [Read 
before 76. Ann. Meet. Brit. Med. Ass., Sheffield, July] <Brit. M. J., 
Lond. (2495), v. 2, Oct. 24, pp. 1249-1251. [Wa, Wm.] 
Bosso, G. [Asst., Lab. parasitol.] 

1895 a. — Sul ciclo evolutivo di talune specie di amebe. [Read 7 giugno] 
<Gior. r. Accad. di med. di Torino, an. 58, 4. s., v. 1 (11), nov., pp. 
650-655. [Wm.] 
Boston, L. Napoleon. [M. D., Bacteriol., Phila. Hosp.] 

1902a. — Tropical dysentery with abscess of liver; rupture into right lung; 
Amoeba coli in the sputum; exhibition of case <Therap. Gaz., Detroit, 
v. 26, 3. s., v. IS (4), Apr. 15, pp. 220-222. [Wa, Wm.] 
Bowman, M. H. [Dr., Bureau Science, Manila, P. I.] 

1901.— Dysentery in the Philippines <N. York M. J. (1385), v. 74 (7), 

Aug. 17, pp. 300-303. [MS. dated June 20.] [Wa, Wm.] 
1901.— Idem <J. Trop. M., Lond., v. 4, Dec. 16, pp. 420-422. [Wa, Wm.] 
1910. — Notes on Amcbae, etc., at Bagnio. [Abstract of paper read before 
Far Eastern Ass. Trop. Med., Manila, Mar. 35] <Med. Rec, N. Y. 
(2002), v. 77 (20), May 14, p. 846; discussion, p. 846. [Wa, Wm.] 
Bradley, C. II. [M. D., Minneapolis, Minn.] 

1905. -Intestinal amebiasis— a case of <Nortbwest. Lancet, Minneapolis, 
v. 25 (13), July 1, pp. 241-242. [Win. I 


Bradley, F. H. [Capt] ; & Smith, F. [Major]. 

1912. — Dysenteric ulceration, without dysenteric symptoms, followed by 
hepatic abscess <J. Roy. Army Med. Corps, Lond., v. 18 (5), May, pp. 
578-579. [Wa, Win.] 

Brannan, John Winters. [M. D., Asst. Path., St. Francis IIosp., New York.] 
3893. — Observations on a case of recurrent amoebic dysentery, with suc- 
cessive large hepatic abscesses <N. York M. J. (747), v. 57 (12), Mar. 
25, pp. 317-319. [Wa, Wm.] 
Brau. [Dr., Med.-Major, l re classe d. troupes colon.] 

1908. — Essai sur la dysenterie amoebienne de Cochinchine <Ann. d'hyg. et 
de ined. colon., Par., v. 11 (4), oct.-dec., pp. 511-547. [Wm.] 

Braun, Maximilian Gustav Christian Carl. [Prof., Zool., Konigsberg i. Pr. ; 

Dr. med. et phil.] 
1883 a. — Die thierischen Parasiten dos Menschon nebst einer Anleitung zur 

praktischen Beschaftigung mit der Helminthologie fiir Studierende und 

Aerzte. viii + 233 pp., 72 figs. 8°. Wiirzburg. [Wa.] 
1893 b. — 2. Bericht iiber thierische Parasiten <Centralbl. f. Bakteriol. 

[etc.], Jena, v. 13 (2), 2S. Jan., pp. 59-68. [Wa, Wm, Wc] 
1895 b. — Die thierischen Parasiten des Menschen. Ein Handbuch fur 

Studirende und Aerzte. 2. Aufl., 283 pp., 147 figs. 8°. Wiirzburg. [Wa.] 
1903.— Idem. 3. vermehrte und verbesserte Aufl. 1 p. 1., [vii]-xii + 3G0 

pp., 272 figs. 8°. Wiirzburg. [Wa.] 
1906. — The animal parasites of man. A handbook for students and medical 

men. 3. enlarged and improved ed. Transl. from the German by Pauline 

Falcke. Brought up to date by Louis W. Sambon & Fred. V. Theobald. 

1 p. 1., [vii]-xix + 453 pp., 294 figs. 4°. London. [Wa.] 
(1906). — I parassiti animali dell' uomo. Trad. ital. 3. ed., 351 pp., figs. 

8°. Milano. 
1908. — Die tierischen Parasiten des Menschen. Ein Handbuch fur 

Studierende und Aerzte. 4. vermehrte und verbesserte Aufl. ix— 475 pp., 

335 figs. Mit einem klinisch-therapeutischen Anhang bearbeitet von Otto 

Seifert. pp. [477]-623. 8°. Wiirzburg. [Wa.] 

Braun, Maximilian Gustav Christian Carl; & Luehe, Max[imilian Friedrich 

1909. — Leitfaden zur Untersuchung der Tierischen Parasiten des Menschen 

und der Haustiere fiir Studierende, Arzte und Tierarzte. vii+186 pp., 

100 figs. 8°. Wiirzburg. [Wa.] 
1910. — A handbook of practical parasitology. Translated by Linda Forster. 

[viii] +208 pp., 100 figs. 4°. London. [Wa.] 

Brem, Walter Y. [Dr., Los Angeles, Calif.] 

1912.— [Discussion of Musgrave, William E., 1912, pp. 13-17] <J. Am. M. 

Ass., Chicago, v. 58 (1), Jan. 6, pp. 17-18. [Wa, Wm, Wc] 
1912.— [Discussion of Smith, Rea, 1912, pp. 300-302] <Calif. State J. M.. 

San Fran., v. 10 (7), July, pp. 302^303. [Wa.] 
Brem, Walter V. ; & Zeiler, A. H. [M. D., Physician, Colon Hosp., Cristobal, 

Canal Zone]. 
1910. — Ipecac in the treatment of intestinal amoebiasis. [Read before Am. 

Soc. Trop. Med., St. Louis, June 11] <Am. J. M. Sc, Phila. & N. Y.. 

n. s. (464), v. 140 (5), Nov., pp. 669-683. [Wm.] 
1911. — The medical treatment of amebic dysentery. [Read at 8. Ann. 

Meet. Am. Soc. Trop. Med., New Orleans, May 18-19] <N. Orl. M. & 

S. J., v. 64 (1), July, pp. 23-42. [Wm.] 


Bristol, Leveret* D. [M. D., Clin. Asst., Med., Univ. Minn., St. Paul.] 

1911. — A case of amebic dysentery <St. Paul M. J., v. 13 (1), Jan., pp. 
30-32. [Wa, Win.] 
Broi'do, S. [Mlle.,^vled. colon., Univ. de Paris.] 

1903. — Des agents pathogenies de la dysenterie <Arch. de ined. exper. et 
anat path., Par., 1. s., v. 15 (6), nov., pp. 820-857. [Wa.] 
Brooks, H. [Dr.] 

1900 a. — [Amoebic colitis.] [Secretary's abstract of report presented be- 
fore N. York Acad. Med., Feb. 20] <Med. News, N. Y. (1418), v. 76 
(11), Mar. 17, p. 433. [Wa, Win.] 
Brown. Alexander G. (jr.). [A. B., M. D., Richmond, Va.] 

1910. — Amebiosis without dysentery. [Read by title before Southside Vir- 
ginia Med. Ass.. Franklin, Oct. 4] <Virginia M. Semi-Month., Rich- 
mond (350), v. 15 (14), Oct. 21, pp. 327-330. [Wa, Win.] 
Brown, W. Carnegie. [M. D., M. R. C. P., London.] 

(1910.) — Amoebic or tropical dysentery: Its complications and treatment. 

1911. — The blood count in amoebic dysentery. [Letter to editor, dated 
July 14] <Brit. M. J.. Lond. (2638), v. 2, July, p. 192. [Wa, Wm.] 

1912. — Some humr ( n entamoebae <Tr. Soc. Trop. M. & Hyg., Lond., v. 5 
(6), Apr., pp. 221-225, 1 pi., figs. 1-3 B. [Wm.] 
Brumpt, E„ 

1909. — [Dysenterie amibienne dans les singes.] [Discussion of Ravaut & 
Dopter, 1909, pp. 17-20] <Bull. Soc. de path, exot., Par., v. 2 (1), 13 
Jan., p. 20. [Wm.] 

1910. — Precis de parasitologic. Preface par R. Blanchard. xxvi+915 pp., 
6S3 figs., 4 pis. 12°. Paris. [Wa.] 
Brunton, (Sir) Lauder. [M. D., F. R. S. ; Physician, Hosp. St. Bartholomew.] 

1903. — A clinical lecture on dysentery and intestinal hemorrhage. Deliv- 
ered at St. Bartholomew's Hospital <Lnncet, Lond. (4166), v. 165, v. 2 
(1), July 4, pp. 7-10, 1 fig. [Wa, Wm.] 
Brunwin, A. D. [M. A., M. B., B. C. Cantab ; Late Resident Med. Officer, Colo- 
nial Hosp., Suva, Fiji.] 

1908. — Some observations on the santonin treatment of dysentery <J. 
Trop. M. & Hyg., Lond., v. 11 (18), Sept. 15, pp. 278-279. [Wa, Wm.] 
Buchanan, Robert Earle. [Ph. D.] 

1911. — Veterinary bacteriology. A treatise on the bacteria, yeasts, molds, 
and Protozoa pathogenic for domestic animals, pp. 9-516, 214 figs. 8°. 
Philadelphia & London. [Wa.] 
Buchanan, W. J. [B. A., M. B. ; Capt. I. M. S.] 

1898. — A note on liver abscess, dysentery, and the Amoeba < Indian M. 
Gaz., Calcutta,, v. 33 (5), May, pp. 165-167. [Wm.] 

1899. — Remarks on the death-rate of dysentery and on dysentery and liver 
abscess <Indian M. Rec, Calcutta, v. 16 (17). Apr. 26, p. 519. [Wm.] 

1900. The saline treatment of dysentery: With notes of 555 consecutive 
cases with 6 deaths <Brit. M. J., Lond. (2041), v. 1, Feb. 10, p. 306. 
[Wa, Wm.] 

1902. — The prevention and treatment of dysentery in institutions in the 
tropics (based on an experience of 1,130 consecutive cases with only nine 
deaths) <Brit M. J., Lond. (2177), v. 2, Sept. 20, pp. 843-844. [Wa, 
Win. | 

L905.— The treatment <>f dysentery. [Editorial] <Indian M. Gaz., Cal- 
cutta, v. 40 (7), July. pp. 279-281. [Wm.] 


Buetschli, Otto. [Prof., Zool., Univ. Heidelberg.] 

1878 a. — Beitriige zur Kenntniss der Flagellaten und einiger verwandten 

Organismen <Ztschr. f. wissensch. Zoo].. Lelpz., v. 30 (2), 22. Jan., 

pp. 205-281, pis. 11-15, figs. 1-26. [MS. dated Aug. 1877.] [Ws.] 
Bunch, Rodney J. [M. D., St. Louis, Mo.] 

1910. — Surgical treatment of amebic dysentery by appendicostomy. [Read 

before 52. Ann. Meet Missouri State Med. Ass., Jefferson City, May, 1009] 

<J. Missouri M. Ass., St. Louis, v. 6 (8), Feb., pp. 474-470; discussion, 

pp. 476-477. [Wm.] 
Bunting, C. H. [M. D., Ass. Path., Johns Hopkins Hosp. Univ.; Path.. Bay 

View Hosp., Baltimore, Md.] 
1906. — Hematogenous amoebic abscess of the lung. Report of a case 

<Arch. f. Schiffs- u. Tropen-Hyg., Leipz., v. 10 (3), Feb., pp. 73-79. 

Bureau, Gustave; & Labbe, Alphonse. 

1908. — Sur l'affection connue sous le nom de botryomycose et son parasite 

<Compt. rend Acad. d. sc, Par., v. 147 (16), 19 oct, pp. 697-699. [Wa, 

Wm, Wa] 
Buttersack. [Dr., Stabsarzt.] 

1902. — Beobachtungen und Untersuchungen liber die Ruhr (Dysenterie). 

Die Ruhrepidemie auf dem Truppeniibungsplatz Doberi'z im Jahre 1901 

und die Ruhr im Osiasiatischen Expeditionskorps. 1. Theil <Veroffentl. 

a. d. Geb. d. Mil.-San.-Wes., Berk, Heft 20, 2 p. 1., pp. 1-61, charts, pis. 

1-7, 3 charts [Wm.] 
Buxton, Joseph. 

1899 a. — Multiple amoebic abscess of the liver without dysentery <Proc. 

Path. Soc. Phila. (1898-99), o. s., v. 20, n. s., v. 2 (3), Jan. 1, pp. 49-51. 

[MS. dated Oct 27, 1898.] [Wm.] 
Cahen, Eugen. [Secundararzt] 

1891 a. — Ueber Protozoen im kindlichen Stuhle <Deu'sche med. Wchnschr., 

Leipz. & Perl., v. 17 (27), 2. Juli, pp. 853-854. [Wa, Wm.] 
Calandruccio, Salvatore. [Dott. med., Lib. Insegnante di zool. ed anat. comp., 

Univ. Catania.] 
1S90 a. — Animali parassiti dell' uoino in Sicilia <Atti Acad. Gioenia di sc. 

nat. in Catania (1889-90), an. 66, 4. s., v. 2, pp. 95-135. [Wa] 
1904. — Appunti di zoologia medica. [Abstract of remarks before Riun. d. 

Cong., 6 apr.] <Rassegna internaz. d. med. mod., Catania, v. 5 (7), 15 

apr., p. 63. [Wm.] 
Caldwell, Robert. [Dr., Nashville, Tenn.] 

1909.— [Discussion of Bates, John Pelham, 1909, pp. 56-59] <J. Tennessee 

State Med. Ass., Nashville, v. 2 (2), June, pp. 60; 63. [Wm.] 
Calkins, Gary Nathan. [Ph. D. ; Instructor, Zool., Columbia Univ.. & Barnard 

College, New York.] 
1901 b.— The Protozoa, xvi+347 pp.,-153 figs. S°. New York. [Wa.Wm.] 
1904. — Evidences of a sexual-cycle in the life-history of Amoeba preteus 

<Arch. f. Protistenk., Jena, v. 5 (1), pp. 1-16, 1 fig., pis. 1-3, figs. 1-27. 

[Wa, Wm.] 
1907.— The Protozoa <Modern Med. (Osier). Phila. & N. Y., v. 1. pp. 353- 

369, figs. 5-10. [Wa, Wm.] 
1907. — The fertilization of Amoeba proleus <Biol. Bull., Lancaster, Pa.. 

v. 13 (4), Sept., pp. 219-230, pis. 11-12, figs. 1-14. [Wa, Wm.] 
1908. — Some Amoeba studies <Am. Naturalist, Lancaster, Pa.. & Garrison. 

N. Y. (498), v. 42, June. pp. 422-428. [Wa, Wa] 


Calkins, Gary Nathan — Continued. 

1909.— Protozoology, pp. iii-ix+17-349, 125 figs., 4 pis. 8°. New York 
& Philadelphia. [Wa.] 
Cannady, Samuel H. [M. D., Oxford, N. C] 

1909. — Case of amebic or dysentery, complicated by abscess of liver < Char- 
lotte [N. C] M. J., v. 59 (6), June, pp. 359-360. [Win.] 
Canney, Fredrick G. [M. D., San Francisco, Calif.] 

1902 a.— Parasitic amebae <Med. News, N. Y. (1555), v. 81 (18), Nov. 1, 
pp. 825-826, figs. 1-5. [Wa.] 

Cantlie, James. [M. B., F. R. C. S.] 

1902. — [Discussion on dysentery] <Brit. M. J., Loud. (2177), v. 2, Sept. 
20, p. 852. [Wa, Wm.] 

Capitanio, Luigi. [Dr.] 

1894 a. — Le amebe rispe to alia patologia <Puglia med., Bari, v. 2 (2), 
feb., pp. 29-36; (3), mar., pp. 61-66; (4-5), apr.-maggio, pp. 99-113. 


Carini, A. 

1912. — Phagedenisnie cutane amibien <Bull. Soc. de path, exot, Par., v. 5 
(4), 10 avril, pp. 216-218. [MS. dated 17 mars.] [Wa, Wm.] 

Casagrandi, Oddo G. V. ; & Barbagallo-Rapisardi, Pietro. 

1895 a. — Richerche biologiche e cliniche sull, Amoeba coli. Nota prelimi- 
nare <Boll. Accad. Gioenia di sc. nat. in Catania, n. s. (39), gennaio, 
pp. 4-14. [Wa] 

1895 c. — Ricerche biologiche e cliniche sull' Amoeba coli (Losch). Seconda 
ed ultima nota preliminare <Ibidem (41), nov., pp. 7-19. [Wa] 

(1895 d). — Sull' Amoeba coli Loesch, ricerche biologiche e cliniche. 15 pp. 
8°. Catania. 

1896 b. — Sui terreni di coltura della amebe. Prima coinunicazione <Ri- 
forma med., Napoli, an. 12 (157), v. 3 (7), 8 luglio, pp. 74-77. [MS. dated 
21 giugno.] [Wm.] 

1S96 c. — Idem. Seconda communicazione <Ibidem (265), v. 4 (40), 16 

nov., pp. 471-473. [Wm.] 
1897 '.— Entamoeba hominis s. Amoeba coli (Losch). Studio biologico e 

clinico <Ann. d' ig. sper., Roma, n. s., v. 7 (1), pp. 103-166, pi. 2. figs. 

1-26. [Wm.] 

1897 a. — Ueber die Kultur von Amoben <Ceiitralbl. f. Bakteriol. [etc.], 
Jena, 1. Abt., v. 21 (15-16), 10. Mai, pp. 579-5S9. [Wa, Wm.] 

Castellani, Aldo. [M. D. ; Director, Bacteriol. Inst., Colombo, Ceylon.] 

(1004). — Dysentery in Ceylon <J. Ceylon Br. Brit. M. Ass.. Colombo, June 

17, pp. 1-14, 1 pi. 
1904. — Some researches on the etiology of dysentery in Ceylon <J. Hyg., 

Cambridge [Eng.], v. 4 (4), Oct., pp. 495-510, 1 fig. [Issued Oct. 1.] 

[Wa, Wm.] 
1905. — Observations on some Protozoa found in human faeces <Centralbl. 

f. Bakteriol. [etc.], Jena, 1. Abt, v. 38 (1), 25. Jan., Orig., pp. 66-69, figs. 

1-5. [Wa, Wm.] 
L905— Diarrhoea from flagellates. [Read before Brit. Med. Ass., Leicester, 

July] <P,rit. M. J., Loud. (2341), v. 2, Nov. 11, pp. 1285-1287, figs. 1-2. 

| Wa, Win. | 
1908.— Note on a liver abscess of amoebic origin in a monkey <Parasi- 

tology. Cambridge ! Kng.], v. 1 (2), June, pp. 101-102, pi. 8. [Issued July 

17.| [Wa.] 


Castellani, Aldo; & Chalmers, Albert J. 

1910. — Manual of tropica] medicine. Univ. ser. xxv+1242 pp., 373 figs., 

14 pis. 8°. London. [Wa.] 
Caullery, Maurice. 

1900. — Sur un amoebien parasite des embryons de Peltogaster curnitux 

Kossm. [Read 13 oct.] <Coinpt. rend. Soc. de biol., Par., an. 58, v. 61, 

v. 2 (28), 19 oct., pp. 266-269, figs. 1-4. [Wa, Wm.] 
Caussade, G. ; & Joltrain, E. 

1907. — Cas de dysenterie amibienne avec abces du foie d'origine pnrisienne 

<Tribune med., Par., n. s., v. 40 (7), 16 few, pp. 101-102; note by Dopter, 

p. 102. [Wm.] 
1907. — Un cas de dysenterie amybienne avec abces du foie d'origine pari- 

sienne. [Read 15 fev.] <Bull. et mem. Soc. med. d. hop. de Par., 3. 

s., v. 24, pp. 167-174; note by Dopter, p. 172; discussion, pp. 174-178. 

1907. — Dysenterie amibienne avec abces hepatique d'origine parisienne. 

[Resume of 1907, pp. 167-174] <Caducee, Par., v. 7 (5), 2 mars. pp. 

62-63. [Wm.] 
Cay ley, Henry. [F. R. C. S. ; Army Med. School, Netley.] 

1893. — Tropical diseases of the liver <Hyg. & Dis. Warm Climates (David- 
son), Edinb. & Lond., pp. 612-640, pi. 3. [Wm.] 
Celli, Angelo. [Dirett, 1st. d'ig., Univ. Roma.] 

1896 b. — Die Kultur der Amoben auf festem Substrate <Centralbl. f. Bak- 

teriol. [etc.], Jena, 1. Abt., v. 19 (14-15), 25. Apr., pp. 536-538. [MS. 

dated 11. Miirz.] [Wa, Wm.] 
Celli, Angelo; & Fiocca, R. 

1894 a. — Contributo alle conoscenze sulla vita delle amebe. l a . Nota pre- 

ventiva <Riforma med., Napoli, an. 10, v. 1 (68), 22 mar., pp. 806-808. 

[MS. dated 10 mar.] [Wm.] 
1894 b. — Idem. 2 a . Communicazione preventiva sulla classificazione delle 

amebe e di alcune specie finora cultivate < Ibidem (187), v. 3 (37), 13 

agosto, pp. 434-^41, 1 table. [Wm.] 
1894 d. — Beitriige zur Amobenforschung. Erste vorliiufige Mitteilung. 

[Transl. of 1894 a] <Centralbl. f. Bakteriol. [etc.], Jena, v. 15 (13-14), 

7. Apr., pp. 470-473. [MS. dated 15. Miirz.] [Wa, Wm, Wc] 

1894 e. — Idem. Zweite vorliiufige Mitteilung. Ueber die Klassifikation der 
Amoben und einige geziichtete Species. [Transl. of 1894 b] < Centra lbl. 
f. Bakteriol. [etc.], Jena, v. 16 (8-9), 6. Sept., pp. 329-339, 1 table. 
[MS. dated 27. Juli.] [Wa, Wm, Wc] 

1895 a. — Intorno alia biologia delle amebe <Ann. 1st. d'ig. sper. Univ. di 
Roma, n. s., v. 5 (2), pp. 177-213, pis. 7-8, figs. 1-67. [Wm.] 

1895 b.— Idem <Bull. r. Accad. med. di Roma, v. 21 (5-6), pp. 285-324, 
pis. 1-2, figs. 1-67. [Wm.] 

1895. — Sulla etiologia della dissenteria. Nota preventiva <Riforma med., 
Napoli, an. 11, v. 1 (34), 9 feb., pp. 399-400. [Wm.] 

1895 d. — Ueber die Aetiologie der Dysenterie. Vorliiufige Mitteilung 
<Centralbl. f. Bakteriol. [etc.], Jena, 1. Abt., v. 17 (9-10), 15. Miirz, pp. 
309-310. [MS. dated 19. Feb.] [Wa, Wm, Wc] 
Chagas, Carlos. [Dr.] 

1911. — Sobre as variagoes ciclicas do cariozoma em duas especies de ciliados 
parazitos. Contribuieao para o estudo do nucleo nos infuzorios. [Portu- 
guese & German text] <Mem. Inst. Oswald Cruz, Rio de Janeiro- 
Manguinhos, v. 3 (1), pp. 136-144, pis. 9-10, figs. 1-18. [MS. dated Jan.] 
66692— vol 2, pt 1—13 14 


Chamberlain, Weston P. ; & Yedder, Edward B. 

1911. — The effect of ultra-violet rays on amoebae, and the use of these 

radiations in the sterilization of water <Philippine J. Sc, Manila, v. 6 

(5), Nov., pp. 383-394, tables 1-6. [Wa.] 
Chantemesse & Rodriguez. 

1909. — Un cas de dysenterie amibienne traite par le lavement creosote* 

<Bull. Soc. de path, exot., Par., v. 2 (1), 13 Jan., pp. 29-32; discussion, 

pp. 32-34. [Wm.] 
Chantemesse & Widal, Fernand. 

18S8 a. — Sur les microbes de la dysenterie <Bull. Acad, de med.. Par., v. 

52, 2. s., v. 19 (16), 23 avril, pp. 522-526; discussion, pp. 528-529. [Wm.] 
Chapin, Charles V. [M. D., Sc. D. ; Supt. Health, Providence, R. I.] 

1910. — The sources and modes of infection. 1. ed. ix+399 pp. 8°. New 

York. [Wa.] 
Charles, (Sir) R. Havelock. [Surg., Bengal Med. Service.] 

1908. — Discussion on tropical abscess of the liver. [Read before 76. Ann. 

Meet. Brit. Med. Ass., Sheffield, July] <Brit. M. J., Lond. (2495), v. 2, 

Oct. 24, pp. 1235-1243; discussion, pp. 1254-1255. [Wa, Wm.] 
Chatton, Edouard. [Preparateur a. l'lnst. Pasteur, Paris.] 

1909. — Une amibe, Amoeba mucicola n. sp., parasite des branches des 

labres, associee a une trichodine <Compt. rend. Soc. de biol., Par., v. 67 

(36), 17 dec, pp. 690-692. [Wa, Wm.] 
1910. — Protozoaires parasites des branchies des labres Amoeba mucicola 

Chatton, Trichodina labrorum n. sp. Appendice : Parasite des trichodines 

<Arch. de zool. exper. et gen., Par., v. 40, 5. s., v. 5 (5), 15 juillet, 

pp. 239-266, 1 fig., pi. 3, figs. 1-26. [Wm.] 
1910. — Essai sur la structure du noyau et la mitose chez les amoebiens. 

Faits et theories <Arch. de zool. exper. et gen., Par., v. 40, 5. s.. v. 5 

(6), l er oct, pp. 267-337, figs. 1-13. [Wm.] 
1912. — Entamibe (Loeschia sp.) et myxomycete (Dictyostelium mucoro'idea 

Brefeld) d'un singe <Bull. Soc. de path, exot, Par., v. 5 (3), 13 mars, 

pp. 180-184, pi. 10, figs. 1-7. [Wa, Wm.] 
1912. — Sur quelques genres d'amibes libres et parasites. Synonymies; 

homonymie; impropriate <Bull. Soc. zool. de France, Par., v. 37 (3), 

25 avril, pp. 109-115; erratum (4), 4 juin, p. 168. [Wa, Wc] 
Chatton, Edouard; & Brodsky, A. [Dr., Univ. de Geneve]. 

1909. — Le parasitisme d'une chytridinee du genre Sphaerita Dangenrd chez 

Amoeba Umax Dujard. Etude comparative <Arch. f. Protistenk., Jena, 

v. 17 (1), pp. 1-18, figs. 1-3. [MS. dated 14 mars.] [Wa, Wm.] 
Chatton, Edouard; & Lalung-Bonnaire, P. 

1912. — Amibe limax (Vahlkampfia n. gen.) dans l'intestin humain. Son 

importance pour l'interpretation des amibes de culture. [Read 14 fev.] 

<Bull. Soc. de path, exot, Par., v. 5 (2), pp. 135-143, pi. 9, figs. 1-17. 

[Wa, Wm.] 
Chauffard, A. 

1908.— [Rapport sur Marcano, G., 1908, pp. 501-505] <Rull. Acad, de med., 

Par., 3. s., v. 59 (18), pp. 501-505; discussion, pp. 505-506. [Wm.] 
1908.— [Discussion of Menetrier, P.; & Touraine, A., 1908, pp. 905-913] 

<Bull. et mem. Soc. med. d. hop. de Par.. 3. s., v. 25, pp. 913-914. [Wm.] 
Chlapowski, F. [Dr.] 

1909.— O dysenteryi pelzakowej (amebowej), z powodu sposl rzoganego 

przypadku. [Amoebic dysentery, apropos of a case.] [Polish text] 

<Now. lek., Poznafi, v. 21 (2), pp. 82-87; (3), pp. 145-147; (6), pp. 

323-329. [Wm.] 



Ciechanowski, Stanislaus [Dr.] ; & Nowak, Julian [Asst, path.-anat Inst., 
Univ. Krakau]. 

1897. — Przyczynek do badan nad etyologia dysentery i <Pam. Towarz. Lek. 
Warszaw., v. 93 (4), pp. 853-924. [Wm.] 

1898 a. — Zur Aetiologie der Dysenterie <Centralbl. f. Bakteriol. [etc.], 
Jena, 1. Abt, v. 23 (11), 17. Mara, pp. 445-452; (12), 25. Mara, pp. 493- 
500, pis. 12-13, figs. 1-3. [Wm.] 
CI egg, Moses T. 

1909. — Some experiments on the cultivation of Bacillus leprae. [Read at 
6. Ann. Meet. Philippine Islands Med. Ass., Feb. 11] <Philippine J. Sc, 
Manila, B. Med. Sc, v. 4 (2), Apr., pp. 77-79; discussion, pp. 141-142. 
Cole, Leon J. 

1908. — Report of the division of animal breeding and pathology <21. Ann. 
Rep. Rhode Island Agric. Exper. Station, Providence (1907-08), pp. 295- 
305. [Wa.] 
Cole, Leon J.; & Hadley, Philip P. 

1910. — Amoeba meleagridis. [Letter to editor] < Science, N. Y., n. s. 
(834), v. 32, Dec. 23, pp. 918-919. [Wa, Wm, Wc] 
Collins, C. C. [Lieut, Asst. Surg., XL S. Army.] 

1904. — [Four cases of amebic dysentery treated with oil] <Rep. Surg.-Gen. 
Army, Wash., pp. 86-87. [Wa, Wm.] 
Cooke, A. B. [M. D., Nashville, Tenn.] 

1909. — [Discussion of Bates, John Pelham, 1909, pp. 56-59] <J. Tennessee 
State M. Ass., Nashville, v. 2 (2), June, pp. 60-62; 63-64; 65. [Wm.] 

1910.— [Discussion of Hanes, (frranville S., 1910, pp. 1140-1146] < Kentucky 
M. J., Bowling Green, v. 8 (1), Jan. 1, pp. 1148-1149. [Wm.] 

1910. — The diagnosis and treatment of amebic ulceration of the large intes- 
tine. [Read before South. Med. Ass., N. Orleans, Nov. 9-11, 1909] 
<J. Am. M. Ass., Chicago, v. 54 (8), Feb. 19, pp. 598-600. [Wa, Wm. Wc] 

1910. — The diagnosis and treatment of amebic ulceration of the large intes- 
tine. [Read before Middle Tenn. Med. Soc, Springfield, Nov. 19, 20] 
<J. Tennessee State M. Ass., Nashville, v. 2 (11), Mar., pp. 325-331. 
Councilman, William T. [Prof., Path., Harvard Med. College, Boston, Mass.] 

1891.— [Discussion of Lafieur, Henri A., 1891 a] < Johns Hopkins Hosp. 
Bull., Bait, v. 2 (13), May-June, p. 84. [Wa, Wm.] 

1891 a. — The form of dysentery produced by the Amoeba coli. [Secretary's 
abstract of paper read before Med. & Chir. State Faculty of Maryland, 
Apr. 28-30] <J. Am. M. Ass., Chicago, v. 16 (23), June 6, pp. 824-825; 
discussion, p. 825. [AYm.] 

1892 b. — Anatomical lesions of amoebic dysentery. [Read Oct. 19, 1S91] 
< Johns Hopkins Hosp. Bull., Bait. (19), v. 3, Jan.-Feb., p. 13. [Wa.] 

1892 c— Dysentery. [Read before Ass. Am. Phys., Wash., May 25] 

<Boston M. &.S. J., v. 127 (1), July 7, pp. 1-7. [Wm.] 
Councilman, William T. ; & Lafieur, Henri A. 

1891 a.— Amoebic dysentery < Johns Hopkins Hosp. Rep., Bait., v. 2 (7-9), 

Dec, pp. 393-548 (156 pp.), pis. 1-7. [Wm.] 
Craig, Charles F. [Acting Asst. Surg., U. S. Army ; Director, Bacteriol. Lab., 

Josiah Simpson, U. S. Gen. Hosp., Fortress Monroe, Va.] 
1901a. — Observations upon the Amoebae coli and their staining reactions 

<Med. News, N. Y. (1470), v. 78 (11), Mar. 10, pp. 414^18, figs. 1-8. 

[Wa, Wm.] 


Craig, Charles F. — Continued. 

1904. — The life cycle of Amoeba coli in the human body: A preliminary 

note <Am. Med., Phila., v. 7 (8), Feb. 20, pp. 299-301, figs. 1-8. 

[Wa, Wm.] 
1904. — The pathology of chronic specific dysentery of tropical origin <J. 

Ass. Mil. Surg. U. S., Carlisle, Pa., v. 14 [(6), June], pp. 353-378. [Wm.] 
1904. — The complications of amoebic and specific dysentery, as observed at 

autopsy. An analysis of one hundred and twenty cases. [Read before 

San Francisco Co. Med. Soc, Feb.] <Am. J. M. Sc, Phila. & N. Y., n. s. 

(388), v. 128 (1), July, pp. 145-156. [Wm.] 
1904. — Classification of Amoeba coli <Am. Med., Phila., v. 8 (5), July 30, 

pp. 185-186. [Wa, Wm.] 
1905. — The etiology and pathology of amoebic infection of the intestine aud 

liver < Interna t. Clin., Phila. & Lond., 14. s., v. 4, pp. 242-298, figs. 1-4, 

pi. 1, figs. 1-12. [Wm.] 
1905. — Observations upon amebas infecting the human intestine, with a de- 
scription of two species, Entamoeba coli and Entamoeba dysenteriae 

<Am Med., Phila., v. 9 (21), May 27, pp. 854-861; (22), June 3, pp. 

897-903; (23), June 10, pp. 936-942. [Wa, Wm.] 
1906. — A new intestinal parasite of man : Paramocba hominis <Am. J. M. 

Sc, Phila. & N. Y., n. s. (413), v. 132 (2), Aug., pp. 214-220, figs. 1-2. 

1908. — Studies upon the amebae in the intestine of man <J. Infec. Dis., 

Chicago, v. 5 (3), June 4, pp. 324-377, pis. 2-3. [Wa, Wm.] 
1910. — Further observations on Pat-amoeba hominis, an intestinal parasite 

of man <Arch. Int. Med., Chicago. ^6 (1), July 15, pp. 1-11, figs. 1-2. 

1911. — The parasitic amoebae of man. x+253 pp., 30 figs. 8°. Philadelphia 

& London. [Wc] 
1911. — Entamoeba tetragena as a cause of dysentery in the Philippine 

Islands <Arch. Int. Med., Chicago, v. 7 (3), Mar., pp. 362-366. [Wm.] 
1912. — Observations upon the morphology of parasitic and cultural amebae 

<J. Med. Research, Bost. (130), v. 26, n. s., v. 21 (1), Apr., pp. 1-37, pis. 

1-2. [Wa, Wm.] 
1912. — The parasitic amebae of man and their relation to disease. [Read 

before 33. Ann. Meet. Louisiana State Med. Soc. Apr. 23-25] <N. Orl. 

M. & S. J., v. 65 (1), July, pp. 1-17. [Wm.] 

Cramer, E. 

1896 a. — Neuere Arbeiten fiber die Tropenruhr oder Amobendysenterie. 
Zusammenfassendes Referat <Centralbl. f. allg. Path. u. path. Anat, 
Jena, v. 7 (4), 29. Feb., pp. 138-145. [Wa, Wm.] 

Crawley, Howard. [S. B., S. M. ; Asst., Zool., Bureau Animal Indust, U. S. 

Dept. Agric, Washington, D. C] 
1912. — The protozoan parasites of domesticated animals <27. Ann. Rep. 

Bureau Animal Indust., U. S. Dept. Agric, Wash. (1910), pp. 465-498, 

figs. 63-75, pis. 37-42. [Wa.] 
1912. — Idem <Circnlar 194, Bureau Animal Indust., IJ. S. Dept. Agric, 

Wash., pp. 465-498, figs. 63-75, pis. 37-42. [Wa.] 

Crivelli, Giuseppe Balsamo; & Maggi, Leopoldo. 

1870 a. — Sulla produzione delle amibe <R. 1st. lomb. di sc. e lett, Rendic, 
Mi la no, 2. s., v. 3 (10), 19 maggio, pp. 367-375, 1 pi., figs. 1-4. [Wm.] 

1871 a.— Idem [continued! <Ibidem, v. 4 (7), 6 apr., pp. 198-203. [Win. | 


Cropper, J. [Dr., Chepstow.] 

1908. — [Tropical abscess of liver.] [Abstract of discussion before 76. Ann. 
Meet. Brit. Med. Ass., Sheffield, July] <Brit M. J., Lond. (2405), v. 2, 
Oct. 24, j). 1254. [Wa, Win.] 

Crowell, S. M. [M. D., Charlotte, N. C] 

1910. — The relation between hookworms, neuraesthenia and morphinism. 
[Read before Seaboard Med. Ass., Norfolk, Va., Dec. 7-9, 1909] <Char- 
lotte [X. C] M. J., v. 01 (2), Feb., pp. 77-79. [Win.] 
Culler, Robert M. [A. M., M. D. ; Capt., Med. Corpus, TJ. S. Army.] 

1910. — Diver abscess. A report of two cases of abscess of the left lobe 
<J. Am. M. Ass., Chicago, v. 55 (6), Aug. 6, pp. 500-501. [Wa, Wm, Wc] 

Cunningham, D. Douglas. [Surg. Major, Special Asst. San. Coinr., Govt. India.] 
1871 a. — A report on cholera <7. Ann. Rep. San. Com. India, Calcutta 

(1870), A pp. B, pp. 141-234, pis. 1-11. [Wm.] 
1881 a.— On the development of certain microscopic organisms occurring in 
the intestinal canal <Quart. J. Micr. Sc, Dond., n. s. (82), v. 21, Apr., 
pp. 234-290, figs. 1-26. pi. 18. [MS. dated Nov., 1879.] [Wa, Wm.] 
Cunningham, John H. (jr.). [M. D., Visit. Surg., Dong Island Hosp., Boston, 
1910. — Death following rectal anesthesia in a patient with amebic dysentery 
<Boston M. & S. J., v. 1G2 (12), Mar. 24, pp. 387-388. [Wm.] 
Curl, Holton C. [M. D., Surg., U. S. Army; Supt, Colon Hosp., Isthmus of 
1906. — The relative value of cecostomy and appeudostomy in the treatment 
of amebic dysentery by irrigation of the colon <Ann. Surg., Phila., v. 43 
(4), Apr., pp. 543-546, 1 pi., fig. 1. [Wm.] 
Curnow, John C. [M. D., Dondon; Prof., Anat, King's College.] 

1895 a. — Hepatic abscess followed by amoebic dysentery; operation; re- 
covery <Dancet, Dond. (3740), v. 1, May 4, pp. 1109-1111, 2 figs., 1 
table. [Wm.] 
Curry, Joseph J. [Asst. Surg., U. S. Army.] 

1901 a. — Dysenteric diseases of the Philippine Islands, with special refer- 
ence to the Amcba coli as a causative agent in tropical dysentery <Bos- 
ton M. & S. J., v. 144 (8), Feb. 21, pp. 177-178. [Wm.] 
Curtice, Cooper. [D. V. S., M. D. ; Veterinary Inspector, Bureau Animal In- 
dustry, Norfolk, Va,] 
1907. — The rearing and management of turkeys with special reference to the 
" blackhead " disease <Bull. 123, Rhode Island Agric. Exper. Station, 
Providence, Aug., 64 pp. [Wa.] 
1907. — Further experiments in connection with the blackhead disease of 
turkeys <Bull. 124, Rhode Island Agric. Exper. Station, Providence, 
Nov., pp. 65-105. [Wa.] 
Czerny, Vinzenz. [Asst. Arzt.] 

1869 a. — Einige Beobachtnngen fiber Amoeben <Arch. f. mikr. Anat., Bonn, 
v. 5, pp. 158-163. [Wm.] 
Daland, Judson. [M. D. : Instructor, Clin. Med. & Decturer, Phys. Diag. & 
Symptomat., Univ. Pennsylvania.] 
1892. — A clinical description of dysentery as it occurs in Nicaragua. [Read 
before Phila. Co. Med. Soc, Oct. 26] <Therap. Gaz., Detroit, Mich., & 
Phila., Pa., v. 16, 3. s., v. 8 (12), Dec. 15, pp. 806-808. [Wm.] 


Daniels, C[harles] W[ilberforce]. [M. B., M. R. C. S. ; Colonial Med. Serv., 
British Guiana.] 
1902 b. — Notes on malaria and other tropical diseases during the tour of the 
Royal Commission on malaria <Brit. Guiana M. Ann., Demerara, pp. 
40^6. [Win.] 
Daniels, CLharles] W[ilberforce] ; & Stanton, A. T. 

1907. — Studies in laboratory work. 2. ed., thoroughly revised, xiv+491 
pp., 156 figs., 4 pis. 8°. Philadelphia. [ Wm.] 
Daniels, C[harles] W[ilberforce] ; & Wilkinson, E. 

1909. — Tropical medicine and hygiene. Part 1 : Diseases due to Protozoa, 
iv pp., 1 p. 1., 2G4 pp., 62 figs., 2 pis. 8°. London. [Wa.] 
Darling, Samuel T. [Ancon, Canal Zone.] 

1912. — Romanowsky stain for entamebas. [Letter to editor] <J. Am. M. 

Ass., Chicago, v. 59 (4), July 27, p. 292. [Wa. Wm. Wc] 
1912. — The examination of stools for cysts of Entamoeba tetragena <J. 
Trop. M. & Hyg., Loud., v. 15 (17), Sept. 2, pp. 257-259. [Wa, Wm.] 
Darnall, Carl R. [First Lieut, Asst, Surg., U. S. Army.] 

1901. — Amoebic abscess of the liver, with a report of four cases <N. York 

M. J. (1158), v. 73 (6), Feb. 9, pp. 229-232. [Wa, Wm.] 
1901. — Amoebic abscess of liver. [Operation] <Rep. Su"rg.-Gen. Army, 
Wash., p. 286. [Wa, Wm, Wc] 
Davaine, Casimir-Joseph. [Dr., Membre, Soc. de biol., Laureat de l'lnst.] 

1877 a. — Traite des entozoaires et des maladies vermineuses de l'homme et 
des animaux domestiques. 2. ed., cxxxii+1003 pp., 72+38 figs. 8°. 
Paris. [Wa.] 

1906.— [Discussion of Juergens, 1906, pp. 1607-1608] <Berl. klin. 
Wchnschr., v. 43 (50), 10. Dec, pp. 1608-1609. [Wa, Win.] 
Davidson, Andrew. [M. D., F. R. C. P. Edinb.] 

1907.— Amoebic dysentary <Syst. Med. (Allbutt & Rolleston), Lond., v. 2 

(2), pp. 527-530; 535-542. [Wm.] 
1907. — Tropical abscess of the liver <Ibidem, pp. 579-605. [Wm.] 
1909.— Amoebic dysentery <Ibidem, v. 2 (2), pp. 527-530; 535-542. [Wa.] 
1909. — Tropical abscess of the liver <Ibidem, pp. 579-605. [Wa.] 
Davidson, D. M. [Surg..-Capt., I. M. S. ; M. B., C. M.] ; & Davidson, Andrew. 
1893. — Dysentery <Hyg. & Dis. Warm Climates (Davidson), Edinb. & 
Lond., pp. 546-611, figs. 47-49. [Wm.] 
Deeks, W. E. [M. A., M. D. ; Chief, Med. Clin., Ancon Hosp., Panama] 

1908. — Preliminary note on the treatment of amebic dysentery as con- 
ducted on the Isthmus of Panama <Med. Rec, N. Y. (19S8), v. 74 (24), 
Dec 12, p. 1010. [Wa, Wm.] 
Deeks, W. PI; & Shaw, W. F. [M. D. ; Physician, Ancon Hosp.]. 

1909. — The treatment of amebic dysentery- [Read before Canal Zone Med. 
Soc, Aug.] <Med. Rec, N. Y. (2036), v. 76 (20), Nov. 13, pp. 806-810. 
[Wa, Wm.] 
191 I.- -Amebic colitis (amebic dysentery). [Read at 8. Ann. Meet. Am. Soc. 
Trop. Med., New Orleans, May 18-19] <N. Orl. M. & S J., v. 64 (1), 
July, pp. 1-23. [Wm.] 
Delafield, Francis [M. I).; Prof., Pract. Med., Coll. P. & S., Columbia Univ.] ; & 
Prudden, T. Mitchell [M. D. ; Prof., Path.; Director, Lab. Histol., Path., 
Bacterid., College P. & S., Columbia Univ., New York]. 
1897 a.— A handbook of pathological anatomy, with an introductory section 
on post-mortem examinations and the methods of preserving and exam- 
ining diseased tissues. 5. ed., 846 pp., 365 figs. 8°. London. [Wa.J 


Dela field, Francis — Continued. 

1001. — A handbook of pathological anatomy and histology. With an intro- 
ductory section on post-mortem examinations and the methods of preserv- 
ing and examining diseased tissues. 6. ed., xix+810 pp., 453 figs., 13 pis. 
8°. New York. [Wa.] 

Denier, A. 

1912. — Un cas de dysenterie mixte provenant de Shang-Hai <Bull. Soc. 
de path, exot., Par., v. 5 (7), 10 juillet, pp. 468-469. [Wa, Wm.] 

Denier, A. ; & Huet. 

1912. — La dysenterie k Saigon <Bull. Soc. de path, exot., Par., v. 5 (5), 8 
mai, pp. 263-265. [Wa, Wm.] 

Diamond, I. B. [M. D., Chicago, 111.] 

1900a.— Amebic dysentery <Phila. M. J. (110), v. 5 (14), Apr. 7, pp. 
817-S20, 1 fig. [Wa, Wm.] 

Dievitski, V. S. 

1003. — Pechenochnii naryv pri tropicheskoi dizcnterii s amebami v gnoie. 
[Liver abscess in tropical dysentery with amebae in the pus.] [Russian 
text] <Med. Obozr., Mosk., v. 59 (10), pp. 774-785. [Wm.] 

Dobell, C, Clifford. [B. A., Trinity College.] 

1008. — On the intestinal protozoan parasites of frogs and toads. (Prelimi- 
nary communication) <Proc. Cambridge [Eng.] Phil. Soc. (1007), v. 14 
(4), Mar. 10, pp. 428-433. [Wa.] 

1909. — Researches on the intestinal Protozoa of frogs and toads < Quart. J. 
Micr. Sc, Loud., n. s. (210), v. 53 (2), Jan., pp. 201-277, 1 fig., pis. 2-5, 
figs. 1-07. [Wa.] 

1909. — Chromidia and the binuclearity hypotheses: A review and a criti- 
cism <Quart. J. Micr. Sc, Lond., n. s. (210), v. 53 (2), Jan., pp. 270-326, 
figs. 1-25. [MS. dated Aug., 1008.] [Wa.] 

1909. — Physiological degeneration and death in Entamoeba ranarum 
<Ibidem (212), v. 53 (4), July, pp. 711-721, figs. A-E. [MS. dated Apr.] 
[Wa, Wm.] 
Dock, George. [M. D. ; Prof., Theory & Pract. Med., Tulane Univ., New Or- 
leans, La.] 

1891 e. — Observations on the Amoeba coll in dysentery and abscess of the 
liver. [Read before Austin Dist. Med. Soc, Mar. 19] <Daniel's Texas 
M. J. Austin, v. 6 (10), Apr., pp. 419-431. [Wm.] 

1902 a. — Amebic dysentery in Michigan. [Read at 53. Ann. Meet. Am. Med. 
Ass.] <J. Am. M. Ass., Chicago, v. 39 (11), Sept. 13, pp. 617-619; dis- 
cussion, pp. 619-620. [Wa, Wm.] 

1900. — A. note on the ipecac treatment of amoebic dysentery. [Read at 6. 
Ann. Meet. Am. Soc Trop. Med., Wash., D. C, Apr. 10] <N. York M. J. 
[etc.] (1597), v. 90 (2), July 10, pp. 49-50; discussion, p. 93. [Wa, 
Wm, Wc] 

1900. — Amebic dysentery. [Read before Orleans Parish Med. Soc, May 10] 
<N. Orl. M. & S. J., v. 62 (2), Aug., pp. 81-S6. [Wni.] 

1909.— [Discussion of Simon, Sidney K., 1909, pp. 1526-1529] <J. Am. M. 
Ass., Chicago, v. 53 (19), Nov. 6, pp. 1529-1530. [Wa, Wm, Wc] 
Dock, George; & Lyons, Randolph [M. D., New Orleans, La.]. 

1910. — Experiments and clinical observations on the effects of ipecac on 
amebae <Tr. Ass. Am. Physicians, Phila. (25. sess., Wash., D. C, May 
3-5), v. 25, pp. 515-527. [Wa, Wm.] 


Dofleiu, Franz. [Dr. phil., a. o. Prof., Zool., Univ. Munchen.] 

1901 a. — Die Protozoen als Parasiten und Krankkeitserreger, nach bio- 
logischen Gesichtspimkten dargestellt. xiii+274 pp., 220 figs. 8°. Jena. 

1902 c. — Das System der Protozoen <Arch. f. Protistenk., Jena, v. 1 (1), 
pp. 169-192, figs. A-C. [MS. dated Dec. 1901.] [Wa, Win.] 

1907. — Sutdien zur Naturgeschichte der Protozoen. 5. Amobenstudien. 

Erster Teil < Ibidem, Suppl. 1, Festbd. z. 25jahr. Prof.-Jubil. Richard 

Hertwig, pp. 250-293, figs. A-R, pis. 17-19, figs. 1-57. [Wm.] 
1909. — Lehrbuch der Protozoenkunde. Eine Darstellung der Naturge- 
schichte der Protozoen mit besonderer Beriicksicktigung der parasitischen 

und pathogenen Formen. 2. Aufl. der Protozoen als Parasiten und 

Krankheitserreger. x+914 pp., 825 figs. 8°. Jena. [Wa.] 
1911. — Idem. 3. stark vermehrte Aufl. xii+1043 pp., 951 figs. 8°. Jena. 

Doflein, Franz ; & von Prowazek, St. 

1903. — Die pathogenen Protozoen (mit Ausnahme der Hamqsporidien) 

<Handb. d. path. Mikroorganism. (Kolle & Wassermann), Jena, v. 1, 

11.-12. Lief., pp. 865-1006, figs. 1-81. [Wa.] 
Dopter, Charles Henri Alfred. [Dr., Med. -major de 2 e classe ; Prof, agrege libre 

du Val-de-Grace.] 
1904. — Transmissibilite de la dysenterie amibienne en France; importance 

de 1'examen bacteriologique dans tout cas de dysenterie <Presse med M 

Par., v. 12 (89), 5 now, pp. 705-707, figs. 1-2. [Wm.] 
1905. — Ueber in Frankreich vorgekommene Uebertragung von Ainoben- 

dysenterie. [Secretary's abstract of paper read before Soc. med. d. hop., 

Par., 28 oct. 1904] < Munchen. med. Wchnschr., v. 52 (2), 10. Jan., p. 99. 

[Wa, Wm.] 
1905. — Effets experimentaux de la toxine dysenterique sur le systeme ner- 

veux <Ann. de l'lnst. Pasteur, Par., v. 19 (6), 25 juin, pp. 353-366, pi. 12, 

figs. 1-2. [Wa, Wm.] 
1905. — Sur quelques points relatifs a Taction pathogene de l'amibe dysen- 
terique <Ann. de l'lnst. Pasteur, Par., v. 19 (7), 25 juillet, pp. 417-425, 

pi. 13, figs. 1-3. [Wa, Wm.] 
1907. — Note histologique fournie. [See Can.ssade & Joltrain, 1907, pp. 

167-174; and 1907, pp. 101-102.] [Read 15 few] <Bull. et mem. Soc. 

mem. d. hop. de Par., 3. s., v. 24, p. 172. [Wm.] 
1907.— Idem <Tribune med., Par., n. s., v. 40 (7), 16 fev., p. 102. [Wm.] 
1907. — [Discussion of Caussade & Joltrain, 1907, pp. 167-174. [15 fev.] 

<Bull. et mem. Soc. med. d. hop. de Par., 3. s., v. 24, pp. 176-177; 178. 

1907. — Dysenterie <Prat. med.-chir., Par., v. 2, pp. 561-570, figs. 77-78. 

1907. — Anatomie pathologique de la dysenterie amibienne <Arch. de med. 

exper. et d'anat. path., Par., 1. s., v. 19 (4), juillet, pp. 505-541, figs. 1-9, 

pis. 13-15. [Wa, Wm.] . 
1908. — Traitenient de la dysenterie amibienne par la creosote. [Read 12 

fev.] <Bull. Soc. de path, exot, Par., v. 1 (2), pp. 68-71; discussion, pp. 

71-72. [Wm.] 
L909. — Traitement de la dysenterie amibienne <Progres med., Par. (44), 30 

OCt, pp. 553-555. [Win.] 
1910.- -Lea dysenteries epidemiologic anatomic pathologique, clinique et 

therapeutique. 210 pp., 5 figs. 12°. Paris. [Wa.] 


Dopter, Charles Henri Alfred — Continued. 

1910. — Treatment of amoebic dysentery < Interna t. Clin., Phila. & Lond 

20. s., v. 2, pp. 32-40. [Wm.] 
Drigalski. [Dr., Stabsarzt] 

1902. — Untersuchimgen. (In Beobachtungen und Untersuchungen iiber die 
Ruhr (Dysenterie). Die Ruhrepidemie auf dem Truppeniibungsplatz 
Doberitz im Jabre 1901 und die Ruhr im Ostasiatisehen Expeditionskorps) 
<Veroffentl. a. d. Geb. d. Mil.-San.-Wes., Berl., Heft 20, pp. 86-109. 
Duncan, Andrew. [M. B., B. S., M. D., F. R. C. P., F. R. C. S.] 

1902.— A discussion on dysentery <Brit. M. J., Loud. (2177), v. 2. Sept. 20, 

pp. 841-843. [Wa, Wm.] 
1912.— Amoebic dysentery <J. Trop. M. & Hyg., Lond., v. 15 (2), Jan. 15, 

pp. 24-25. [Wa, Wm.] 
1912. — Amoebic dysentery <J. Lond. Scbool Trop. Med., v. 1 (2), Mar., 
pp. 149-152. [Wa.] 
Dunglison. Robley. [M. D., LL. D. ; Prof., Jefferson Med. College, Philadel- 
phia, Pa. | 
1893 a. — Medical lexicon. A dictionary of medical science [etc.]. Revised 
by Richard J. Dunglison. 21. ed., xi+1181 pp. 4°. Philadelphia. [Wm.] 
1895 a.— Idem. 21. ed., xi+1206 pp. 4°. Philadelphia. [Wm.] 
Duval, H. Rubens; & Lemarchal, R. 

1910. — Cellules simulant des amibes et cancer a evolution anormale <Arch. 
de parasitol., Par., v. 14 (2), 30 oct, pp. 319-329, figs. 1-3. [Wa.] 
Earle, Samuel T. [Dr.] 

1905. — Amoebic dysentery — cold water and antiseptic treatment. [Read 
before Baltimore Med.-& Surg. Ass., Nov. 14, 1904] < Virginia M. Semi- 
Month., Richmond (213), v. 9 (21), Feb. 10, p. 498; discussion, pp. 
498-499. [Wa.] 
Ebstein, Ludwig. [Dr., Volontararzt, med. Klinik.] 

1901 a. — Ueber einen Protozoenbefund in einem Falle von acuter Dysenterie 
<Arch. f. exper. Path. u. Pharmakol., Leipz., v. 46 (5-6), 3. Oct., pp. 448- 
458, pi. 2, figs. 1^. [Wa.] 
Edwards, William A.; & Waterman, James Sears. 

1892 a. — Hepatic abscess; report of a case, with remarks upon the Amoeba 
coli <Pacific M. J., San Fran., v. 35 (3), Mar., pp. 129-141, figs. 1-3. 
Eichberg, Joseph. [Prof., Physiol., Univ. Cincinnati.] 

1891 a. — Hepatic abscess and the Amoeba coli. [Read before Cincinnati 
Med. Soc, Feb. 3] <Med. News, Phila. (971), v. 59 (8), Aug. 22, pp. 
201-205. [Wa, Wm.] 
Eichhorst, Hermann Ludwig. [Prof., Special Path. & Therap. ; & Director, Med. 
Clin., Univ. Zurich. ] 
1901 a. — A text-book of the practice of medicine. [Transl. from German 
by Augustus A. Eshner.] v. 1, 628 pp., 84 figs. 8°. Philadelphia & 
London. [Wm.] 
Ellis, John W. [M. D., Ph. G., Lampasas, Texas.] 

1907. — Report of a case of amoebic dysentery <Texas Cour.-Rec. Med., 
Fort Worth, v. 24 (0), Feb., pp. 1-2. [Wm.] 
Elmassian, M. [Dr.] 

1909. — Sur V Amoeba blattae. Morphologie generation <Arch. f. Protistenk., 
Jena, v. 16 (2), pp. 143-163, figs, a-g, pi. 11, figs. 1-33. [MS. dated Nov.. 
1908.] [Wa, Wm.] 


Elmassian, M. — Continued. 

1909. — Snr une nouvelle espece ainibienne chez l'homine, Entamoeba minuta 
n. sp. l ro memoire. Morphologie-evolution-pathogeiie <Centralbl. f. Bak- 
teriol. [etc.], Jena, 1. Abt., v. 52 (3), 19. Nov., Orig., pp. 335-351, 2 pis. 
[Wa, Win.] 
Engelmann, Theodor Wilhelm. [Dr. med., o. Prof., Physiol., Univ. Berlin; 
Editor, Arch. f. Physiol.] 
1869 a. — Over electrische prikkeling van Amoeba en Arcella <Onderzoek. 
ged. in h. physiol. Lab. d. Utrecht. Hoogesch., 2. s., v. 2, pp. 430-443, 
1 fig. [Wm.] 
Entz, Geza. [Dr., Jun.] 

1912. — Ueber eine neue Amobe auf Siisswasser-Polypen (Hydra oligactis 
Pall.) <Arch. f. Protistenk., Jena, v. 27 (1), 5. Oct., pp. 19-47, figs. 1-2, 
pis. 2-3, figs. 1-19. [Wa, Wm.] 
Epstein, Alois [Prof., Prag.] 

1893 a. — Beobachtungen iiber Monocercomonas hominis (Grassi) und 
Amoeba coli (Loesch) bei Kinder-Diarrhoen <Prag. med. Wchnschr., 
v. 18 (38), 20. Sept., pp. 463-465; (39), 27. Sept., pp. 475-476, figs. A-B ; 
(40), 4. Oct., pp. 486^88. [Wm.] 
Erdmann, Rh. [K. Inst. f. Infektionskr., Berlin.] 

1910. — Depression und fakultative Apogamie bei Amoeba diploidea 
<Festschr. z. 60. Geburtst. Richard Hertwigs (Miinchen), Jena, v. 1, pp. 
323-348, figs, a-e, pis. 25-26. [Wm.] 
Fajardo, Francisco. [Dr. ; Direktor, Lab. bacteriol. federal, Rio de Janeiro.] 
1896 a. — Ueber amobische Hepatitis und Enteritis in den Tropen (Bra- 
silien) <Centralbl. f. Bakteriol. [etc.], Jena, 1. Abt., v. 19 (20),. 4. Juni, 
pp. 753-768, figs. 1-10. [Wa, Wm.] 
Fantham, H. B. [D. Sc. Lond., B. A. Cantab., A. R. C. S.] 

1910. — Observations on the parasitic Protozoa of the red grouse (Lagopus 
scoticus). [Secretary's abstract of 1910, pp. 692-708] <Abstr. of Proc. 
Zool. Soc. Lond. (84) [May 10], p. 30. [Wa.] 
1910. — Observations on the parasitic Protozoa of the red grouse (Lagopus 
scoticus), with a note on the grouse fly. [Read May 3] <Proc. Zool. 
Soc. Lond. (3), Oct., pp. 692-708, pis. 59-61, figs. 1-65. [Wa.] 
1911. — On the amoebae parasitic in the human intestine, with remarks on 
the life-cycle of Entamoeba coli in cultures <Ann. Trop. M. & Parasitol., 
Liverpool, ser. T. M.. v. 5 (1), Apr. 20, pp. 111-123. [Wa, Wm.] 
Fantham, H. B. ; & Porter, Annie. 

1911. — A bee-disease due to a protozoal parasite (Nosema apis). [Exhibi- 
tion with remarks, Apr. 4] <Proc. Zool. Soc. Lond. (3), Sept., pp. 625- 
626. [Wa.] 
1912. — Report on the Isle of Wight bee disease (microsporidiosis). Section 
13: Note on certain Protozoa found in bees <J. Bd. Agric, Lond., v. 19 
(2), Suppl. (8), May, p. 138. [Wa.] 
Fearnside, C. F. [M. B., Major I. M. S. ; Med. Supt, Central Prison, Vellore.] 
1905. — Dysentery in the prisons of the Madras Presidency <Indian M. Gaz., 
Calcutta, v. 40 (7), July, pp. 241-247, charts A-K, 2 tables. [Wm.] 
Feinberg, Ludwlg. [Arzt.] 

1899 a. — Demonstration von Amoeben. [Secretary's abstract of paper read 
before Yer. f. Inn. Med., Berl., 9. Jan.] <Deutsche med. Wchnschr., Leipz. 
& Berl., v. 25 (5), 2. Feb., Ver.-Beilage, pp. 26-27: [Wa, Wm.] 
L899. -Ueber Amdben und ihre Unterscheidung von Korperzellen <Fortschr. 
(1. Med., Berl., v. 17 (4), 15. Feb., pp. 121-127, pis. 1-2. [Wa, Wm.] 


Feldman. [Dr.] 

3912. — Erfahrungen mit Ipekakuanha bei Dysenterie <Arch. f. Schlffs- u. 
Tropen-Hyg., Lelpz., v. 16 (6), Miirz, pp. 192-193. [Wa, Wm.] 
Fenoglio, Ignazio. [Prof., diret., clin. mod.. Cagliari.] 

1890. — Entero-colite par Amoebae coli <Arch. ital. de biol., Turin, v. 14 

(1-2), 6 oct., pp. 02-70. [Wm.] 
[1900]. — Sur Taction pathogene de 1' Amoeba coli <13. Cong. Internat. de 

med. C. r., Par., 2-9 aout, sect, path, interne, pp. 415-419. [Win.] 
1904. — Sull' azione patogena dell' Amoeba coli (enterocolite da Amoeba 
coli) <Giubileo didattico d. Camillo Bozzolo. Raccolta di scrit. med., 
Torino, pp. 245-267. [MS. dated genua io.] [Wm.] 
Fernando, H. Marcus. [Dr., B. Sc. Loud.] 

1904. — On the treatment of dysentery. [Read Nov. 12] <J. Ceylon Br. Brit. 
M. Ass., Colombo, v. 1 (2), July-Dec, pp. 56-60. [Wm.] 
Fiaschi, Thomas. [M. D., Ch. D., Pisa & Florence.] 

1898 a. — Clinical notes on a case of amebic abscess of the liver and lung 
<Anstralas M. Gaz., Sydney (207), v. 17 (12), Dec. 20, pp. 511-512. 
1899. — Clinical notes on a case of amoebic abscess of the liver and lung 
<Indian M. Rec, Calcutta, v. 16 (4), Jan. 25, pp. 109-110; pathological 
notes, by J. L. T. Isbister, pp. 110-111. [Wm.] 
Fieblger, Josef. [Dr. med.] 

1912. — Die tierischen Parasiten der Hans- and Nutztiere. Ein Lehr- und 
Handbucli mit Bestimmungstabellen fiir Tierarzle und Studierende. 
xvi+424 pp.. 302 figs., 1 pi. 8°. Wien & Leipzig. [Wa.] 
Fink, Lawrence G. [M. B., C. M. Edinb.] 

1912. — Liver abscess treated by a modification of the Leonard Rogers' 

method <J. Trop. M. & Hyg.. Lond., v. 15 (22), Nov. 15, pp. 339-340. 

[Wa, Wm.] 

Finley, Frederick Gault [M. D., London] ; & Adami, J. George [M. D., Montreal]. 

1894 a. — Amoebic abscess of the liver <Montreal M. J., v. 22 (10), Apr.. 

pp. 728-731. [Wm.] 
1895.— Amoebic abscess of the liver. [Remarks, Feb. 23. 1S94] <Proc. 
Montreal Med.-Chir. Soc. (1892-94), v. 7 pp. 375-378; discussion, pp. 
378-379. [Wm.] 
Finley, Frederick Gault; & Wolbach, S. B. [M. D., Montreal]. 

1910. — A case of amoebic dysentery with abscess of the liver, originating in 
Montreal <Montreal M. J., v. 39 (6), June, pp. 389-394. [Wm.] 
Fiori, Telesforo. [Dr.] 

1S96 a. — Sulla vita delle amebe dell'mtestino dell'uomo sano e malato <Ann. 
d'ig. sper., Roma, n. s., v. 6 (4). pp. 467-473, 2 pis. [MS. dared 25 mar.] 
Fisch, R. 

1904. — Leber die Behandlung der Amobendysenterie und einige andere 
tropenmedizinische Fragen <Arch. f. Schiffs- u. Tropen-Hyg., Leipz., 
v. 8 (5), Mai, pp. 207-212. [Wm.] 
Flexner, Simon. [ M. D. ; Prof., Path., Univ. Penn., Phila., Pa.: Director, Rocke- 
feller Inst, for Infec. Dis., New York.] 
1892 c. — Amoebae in an abscess of the jaw < Johns Hopkins Hosp. Bull,. 

Bait. (25), v. 3, Sept., pp. 104-106. [Wa, Wm.] 
1896 a. — A c;ise of combined protozoan and bacterial infection. Amoebic 
dysentery, malaria, and Micrococcus lanceolatus, acute fibrino-purulent 
peritonitis < Johns Hopkins Hosp. Bull., Bait. (66-67), v. 7. Sept.-Oet., 
pp. 171-173. [Wa.] 


Flexner, Simon — Continued. 

1897 b. — Perforation of the inferior vena cava in amoebic abscess of the 
liver <Am. J. M. Sc, Phila. & N. Y., n. s. (301), v. 113 (5), May, pp. 
553-558. [Wm.] 

1900. — Dysentery. [Abstract of paper read before 51. Ann. Meet. Am. 
Med. Ass., Atlantic City, N. J., June 5] <Phila. M. J., v. 5 (23), June 
9, p. 1262. [Wa, Wm.] 

1900 a. — Etiology of dysentery. Chronic dysentery. Prospects of im- 
munity and cure. [Secretary's abstract of paper read before 51. Ann. 
Meet. Am. Med. Ass., Atlantic City, N. J., June 5] <Med. News, N. Y. 
(1430), v. 76 (23), June 9, pp. 930-931. [Wa, Wm.] 

1900 b. — On the etiology of tropical dysentery. Middleton-Goldsmith lec- 
ture, delivered before the New York Pathological Society, April 12, 
1900 <Phila. M. J., v. 6 (9), Sept. 1, pp. 414-424. [Wm.] 

1900 c. — The etiology of tropical dysentery. [Same as 1900 b, abridged] 
<Brit. M. J., Loud. (2074), v. 2, Sept. 29, pp. 917-920. [Wa, Wm.] 

1900. — The etiology of tropical dysentery <Centralbl. f. Bakteriol. [etc.], 
Jena, 1. AM., v. 28 (19), 30. Nov., pp. 625-631. [Wa, Wm.] 

1901. — On the etiology of tropical dysentery. Middleton-Goldsmith lecture 
<Proe. N. York Path. Soc. (1899-1900), pp. 297-337. [Wm.] 

1901. — Etiology of dysentery- [Read before 51. Ann. Meet. Am. Med. Ass., 
Atlantic City, N. J., June 5-8, 1900] <J. Am. M. Ass., Chicago, v. 36 
(1), Jan. 5, pp. 6-10. [Wa, Wm, Wc] 

1901.— [Discussion of Harris, H. F., 1901, pp. 191-194] <Proc. Path. Soc. 
Phila., o. s., v. 22, n. s., v. 4 (8), June 1, pp. 194-196. [Wm.] 

1907. — Amoeba — amoebae of the intestinal canal in man <Syst. Med. (All- 
butt & Itolleston), Lond., v. 2 (2), pp. 530-535. [Wm.] 

1909.— Amoeba <Ibidem, pp. 530-535; 542-544. [Wa.] 
Forster, W. H. C. [M. B., C, M., Capt.] 

1907. — A preliminary note on the application of vaccinotherapy to dysen- 
tery <Indian M. Gaz., Calcutta, v. 42 (6), June, pp. 201-204. [Wm.] 

1906. — x\moben- und bakterieller Dysenterie. [Secretary's abstract of 
paper read before Biol. Abt. d. Aerztl. Ver., Hamburg, 13. Marz] 
<Munchen, med. Wchnschr., v. 53 (25), 19. Juni, p. 1232. [Wa, Wm.] 
Franca, C. ; & Athias, M. 

1906. — Recherches sur les trypauosomes des amphibiens <Arch. r. Inst. 
bacterid. Camara Pestana, Lisb., v. 1 (1), mai, pp. 127-165, figs. 1-25, 
pi. 3, figs. 4-17; pi. 4, figs. 1-12. [Wa.] 
Franchini, G. [Dr., Asst. e libero Doc] 

1911. — Iiiproduzione sperimentale della dissenteria tropicale da Entameba 
nella scimmia <Malaria e mal. d. paesi caldi, Roma, v. 2 (7), luglio, pp. 
189-195, 1 fig., 1 pi., figs. 1-2 ; resume in French & English, p. 195. [Wm.] 

1911. — Sull azione patogena del]e amebe da fieno nei conigli <Ibidem (10), 
ott., pp. 291-294; resume in French & English, pp. 294-295. [Wm.] 
Franchini, G. ; & Raspaolo, D. G. 

1911. — Sulla coltivabilita delle amebe da fieno <Malaria e mal. d. p; 
caldi, Roma, v. 2 (5), maggio, pp. 130-136, 1 pi., figs. 1-4; resume in 
French & English, p. 336. [MS. dated maggio.] [Wm.] 

1911. — Amoebendysentei Le. 1 Secretary's abstract of paper read before Wis- 
asch. Ver <l. Mil.-Arzte d. Garnison, Wien, 12. Nov. 1910] <l)eulsche 
med. Wchnschr., Leipz., v. 37 (10), 9. Miirz, p. 480. [Wa, Wm.] 


B'reer, Paul C. [M. I)., Ph. D.] 

1902. — Ti'O preparation of benzoyl-acetyl peroxide, and Ita use as an 
tinal antiseptic in cholera and dysentery. Preliminary notes <[P 
t i <>ii] (2), Bureau Gk)Vt. Lab., Manila, IT pp. [Wa.] 
Freund, Hugo A. [Dr., Detroit, Mich.] 

1909.— [Discussion of Simon, Sidney K., 1909, pp. 1526-1529] <J. Am. M. 
Ass., Chicago, v. 53 (19), Nov. 0, p. 1529. ! Wa, Wm, Wc] 
Frosch. [Geh. Med.-Rat Prof.] 

1909. — Beitrag zur Biologic saprophytischer Amoben <Ztschr. f. Krebs- 
forsch., Berl., v. 8 (2), pp. 183-194, figs. 1-2, pi. 1. [Wm.] 
Frosch, P. [Dr., Asst., Inst. f. Infectionskrankh., Berlin.] 

1897 a. — Zur Frage der Reinziichtung der Amoben. (Vorliiufige Mitteilung) 
<Centralbl. f. Bakteriol. [etc.], Jena, 1. Abt., v. 21 (24-25), 10. Juli, pp. 
920-932. [MS. dated 13. Jnni.] [Wa, Wm.] 
Funkhonser, R. M. [M. D., St. Louis, Mo.] 

1903. — A case of amebic dysentery. [Bead before St. Louis Med. 8oc., Sept. 
26] <St. Louis M. Bev. (1159), v. 48 (20), Nov. 14, pp. 34&-S**, 1 fig.; 
note by Dr. Gradwohl, p. 344; discussion, p. 346. [Wm.] 
Futcher, Thomas Barnes. [M. B., Ass. Med., Johns Hopkins Univ., Baltimore, 

1902 a. — Biology of amebae and white blood-cells. [Abstract of remarks 
before 53. Ann. Sess. Am. Med. Ass., Saratoga Springs, June 10] <Med. 
News, N. Y. (1535), v. SO (24), June 14, p. 1162. [Wa, Wm.] 

1903 d. — A study of the cases of amebic dysentery occurring at the Johns 
Hopkins Hospital. [Read at 54. Ann. Sess. Am. Med. Ass.] <J. Am. M. 
Ass., Chicago, v. 41 (8), Aug. 22, pp. 4S0-488. [Wa, Wm, Wc] 

1909.— [Discussion of Simon, Sidney K., 1909, pp. 1526-1529] <J. Am. M. 

Ass., Chicago, v. 53 (19), Nov. 6, p. 1529. [Wa, Wm, Wc] 
Gabbi, Umberto. [Prof. Dr., Rom.] 

1906. — Sull' etiologia e per la diagnosi di ascesso epatico <Riforma med., 

Napoli, v. 22 (17), 28 apr., pp. 449^59. [Wm.] 
1911. — Dissenteria tropicale da Entameba tetragcna <Malaria e mal. d. 

paesi caldi, Roma, v. 2 (5), maggio, pp. 136-138; resume in French & 

English, p. 138. [MS. dated mar.] [Wm.] 
1911. — Dissenteria tropicale da Entameba tetragena <Path. Riv. quindicin.. 

Genova (60), v. 3, 1° maggio, pp. 203-204. [MS. dated mar.] [Wm.] 
1912. — Ueber Tropenkrankheiten in Suditalien <Centralbl. f. Bakteriol. 

[etc.], Jena, 1. Abt., v. 02 (7), 21. Marz, Orig., pp. 5S0-58S. [Wa, Wm.] 
Gage, John G. [M. D., Ann Arbor, Mich.] 

1909. — A case of amoebic enteritis with Uncinaria, Trichocephalus, and tri- 

chomonads, showing results of treatment after four years <N. York M. J. 

[etc.] (1618), v. 90 (23), Dec. 4, pp. 1106-1109, figs. 1-1. [Wa, Wm.] 
Gallager, Harry. [Dr.] 

1910. — [Treatment of dysentery.] [Abstract of discussion before Delaware 

Co. Med. Soc, Chester, Pa., Feb. 24] <Penn. M. J., Athens, v. 13 (7), 

Apr., p. 574. [Wm.] 
Galloway, James. [M. D., F. R. C. S., M. R. C. P. ; Path., Great North. Centr. 

1894. — Report on the pathology [see Manson, Patrick, 1894, p. 676] <Brit. 

M. J., Lond. (1735), v. 1, Mar. 31, pp. 676-677. [Wm.] 
Gant, Samuel Goodwin. [M. D., LL. D. ; Prof., Rectal & Anal Surg., N. Y. 

Post Grad. Med. School & Hosp.] 
1903 a. — Benign ulcerations of the bowels and anus < Postgraduate, N. Y., 

v. IS (9), Sept., pp. 739-744; discussion, pp. 744-755. [Wm.] 


Gant, Samuel Goodwin — Continued. 

1906. — Appendicostomy and cecostoniy for the relief of chronic diarrhea : 

Report of nine cases. [Read before Am. Proctol. Soc, Boston, June 6] 

<Boston M. & S. J., v. 155 (10), Sept. 6, pp. 258-260. [Wm.] 
1909.— [Discussion of Simon, Sidney K., 1909, pp. 1526-1529] <J. Am. M. 

Ass., Chicago, v. 53 (19), Nov. 6, p. 1531. [Wa, Wm, Wc] 
1910.— [Discussion of Hanes, Granville S., 1910, pp. 1140-1146] <Kentucky 

M. J., Bowling Green, v. 8 (1), Jan. 1, pp. 1147-1148. [Wm.] 
Garin, Ch. [Interne d. hop., Lyon.] 

1910. — La dysenterie amibienne autochtone <Semaine med., Par., v. 30 

(34), 24 aout, pp. 397-398. [Wm.] 
1911. — La dysenterie amibienne autochtone. [Read 22 nov. 1910] <Bull. 

Soc. med. d. hop. de Lyon (1910), v. 9, pp. 420-426. [Wm.] 
1911. — La dysenterie amibienne autochtone <Lyon med., an. 43, v. 116 (1), 

l er Jan., pp. 20-26. [Wm.] 
Gasser, J. [Dr., Med. aide-major, l re classe.] 

1895 a. — Note sur les causes de la dysenterie <Arch. de med. exper. et 

d'anat. path., Par., 1. s., v. 7 (2), l er mars, pp. 198-202. [Wa, Wm.] 
Gauducheau, A. [Dr., Med.-major, T classe hors cadre; Directeur, Inst, vac- 

cinogene du Tonkin.] 
1906.— Reproduction experimentale de la dysenterie amibienne par inocula- 
tion intra veineuse de pus d'abces du foie <Gaz. hebd. d. sc. med. de 

Bordeaux, v. 27 (3), 21 Jan., pp. 25-26. [Wm.] 
1906. — An experimental reproduction of amoebic dysentery by intravenous 

inoculation of pus from a hepatic abscess <J. Trop. M., Lond., v. 9 (4), 

Feb. 15, pp. 52-53. [Wa, Wm.] 
1907. — Note preliminaire sur la culture et la foncion bacteriolytique d'un 

protozoaire amiboide <Gaz. hebd. d. sc. med. de Bordeaux, v. 28 (17), 

28 avril, pp. 195-197. [MS. dated 4 mars.] [Wm.] 
1907. — Culture d'une amibe dysenterique <Ibidem (41), 13 oct, pp. 486-489, 

figs. 1-6. [MS. dated 14 aout] [Wm.] 
190S. — Formation de corps spirillaires dans une culture d'amibe. [Read 

21 mars] <Compt. rend. Soc. de biol., Par., an. 60, v. 64, v. 1 (11), 27 

mars, pp. 493^94. [Wa, Wm.] 
1908. — Presence de protozoaires dans un papier. [Read 13 mai] <Bull. 

Soc. de path, exot., Par., v. 1 (5), pp. 297-298. [Wm.] 
1909. — Sur une culture amibienne <Ibidem, v. 2 (5), 12 mai, pp. 247-252. 

1909. — Idem. Deuxieme note: Etude de l'amibe <Ibidem (7), 21 juillet, 

pp. 370-374. [Wm.] 
1909. — Idem. Troisieme note; Corps spirillaires avec les planches iii et 

iv <Ibidem (10), 8 dec, pp. 568-571, pis. 3-4. [Wm.] 
1911. — Cils geants et corps fuso-spirillaires amibiens <Compt. rend. Soc. 

de biol., Par., v. 70 (5), 10 fev., pp. 172-173. [Wa, Wm, Wc] 
1912. — Researches in the multiplication of the entamoeba e. [Secretary's 

abstract of paper read before 2. bien. Cong. Far East. Ass. Trop. M., 

Hong Kong] <J. Trop. M. & Hyg., Lond., v. 15 (20), Oct. 15, p. 313. 

[Wa. Wm.] 
Gedoelst, L. [Prof., Ecole de med. vet. de l'etat, Bruxelles.] 

1913. — Synopsis do parasitologic de l'homme et des animaux domestiques. 

xx-f-'w2 pp., 327 figs. 8°. Lierre & Bruxelles. [Wa, Lib. Ransom.] 
Gerould, John II. 

1906. — Amoeba blattae and amoeboid motion <Science, N. Y. (592), n. s., 

v. 2.'5. May 4, pp. 707-710. [Wa. Wm, Wc] 


Gerry, B. Peabody. [M. D., Jamaica Plains, Mass.] 

1892 a. — A case of amoebic dysentery. [Rend June 8] <J. Am. M. Ass., 
Chicago, v. 19 (4), July 23, pp. 101-104. [Wm.] 
Gerry, E. Peabody; & Fitz, Reginald H. 

1891 a.— A case of amoebic dysentery <Bos'on M. & S. J., v. 125 (23), Dec. 
3, pp. 592-593. [Wm.] 
Gibbon, John H. [Dr.] 

1902.— Liver abscess, probably of amoebic origin. [Abstract of remarks 
before Phila. Acad. Surg., Mar. 3] <Ann. Surg., Pliila., v. 3G (1), July, 
pp. 148-150. [Wm.] 
1903. — Liver abscess, probably of amoebic origin. [Remarks, Mar. 3, 1902] 
<Tr. Phila. Acad. Surg., v. 5, pp. 53-55. [Wm.J 
Giffard, G. G. [Capt. I. M. S.] 

1907. — Hepatic abscess, and some points in the diagnosis of multiple hepatic 
abscess. [Read before Madras Br. Brit. Med. Ass.] < Indian M. Gaz., 
Calcutta, v. 42 (1), Jan., pp. 14-17; discussion, pp. 17-18. [Wm.] 
Glaeser, Hans. 
1912. — Untersuchungen iiber die Teilung einiger Amoben, zugleich ein Beitrag 
zur Phylogenie des Centrosoms <Arch. f. Protistenk., Jena, v. 25 (1), 
pp. 27-152, figs. 1-5, pis. 3-8, figs. 1-93. [Wa, Wm.] 
Goldlee, Rickman. 

1902 a. — Tropical abscess of the liver. [Secretary's abstract of paper read 
before Roy. M. & Chir. Soc, Lond., May 13] <Brit. M. J., Lond. (2159), 
v. 1, May 17, p. 1210. [Wa, Wm.] 
Goldsmith, F. [Govt. Med. Off., Australia.] 

1901a. — The life cycle of Amoeba dysentcrica <J. Trop. M., Lond., v. 4 
(22), Nov. 15, pp. 372-374. [Wm.] 
Goltman, M. [C. M., M. D., Memphis, Tenn.] 

1903. — The treatment of acute and chronic dyentery. [Read before Tri- 
State Med. Ass. (Miss., Ark. & Tenn.), Memphis, Nov. 12, 1902] <Mem- 
phis M. J., v. 23 (2), Feb., pp. 73-S2. [Wm.] 
1905.— [Discussion of Tuttle, James P., 1905, pp. 348-353] <Lancct-Clink\ 
Cincin., v. 94, n. s., v. 55, Sept. 23, p. 355. [Wm.] 
Goodhue, E. S. [M. D.] 

1906. — Hawaii as a field for scientific work in tropical medicine. [Abridged 
from paper read before Hawaiian Territorial Med. Soc, Honolulu] <J. 
Am. M. Ass., Chicago, v. 46 (21), May 26, pp. 1583-1584. [Wa, Wm.] 
Gottstein, Ernst. [Dr.] 

1903. — Ueber Zuchtung von Amoben auf festen Nahrboden <Hyg. Rund- 
schau, Berl., v. 13 (12), 15. Juni, pp. 593-596. [Wa. Wm.] 

Gould, George M. 

1S91.— The Amoeba coli. [Editorial] <Med. News, Phila., v. 59 (4), July 
25, pp. 107-108. [Wa, Wm.] 
Gradwohl, R. B. H. [Dr.] 

1902.— [Discussion of Nietert, H. L., 1902, pp. 55-61] <St. Louis M. Rev. 

(1091), v. 46 (4), July 26, p. 65. [Wm.] 
1903.— [Note to Funkhouser, R. M., 1903, pp. 343-344] <Ibidem (1159), 
v. 48 (20), Nov. 14, p. 344; discussion, p. 346. [Wm.] 

Graham, Henry Gereon. [M. D., Chicago, 111.] 

1S99 a. — The Amoeba cilia?*ia [ciliata] in disease <N. York M. J. (1087), 
v. 70 (14), Sept. 30, pp. 477-482; (1088) (15), Oct. 7, pp. 515-520. 
[Wa, W T m.] 


Graham, St. Joseph B. [M. D. ; Co-editor, Georgia J. M. & S., Savannah.] 

1900 a. — A preliminary report of the discovery of Ameba and Plasmodia in 

cultures from the blood of persons suffering with malaria and paludal 

fevers, and the discovery of motile bodies in human blood-plasma and 

their growth in pure culture, with some remarks pertaining to the sub- 
ject. [Read before Georgia M. Ass., Apr., 1899] <Georgia J. M. & S., 

Savannah, v. 6 (2), Feb., pp. 55-58. [Win.] 
Graser, H. R. A. [Dr.] 

1900 a. — Amoebic colitis. [Secretary's abstract of report before N. York 

Acad. Med., Feb. 20] <Med. News, N. Y. (1418), v. 76 (11), Mar. 17, 

p. 433. [Wa, Win.] 
1900. — Amoebic dysentery in animals. [Secretary's abstract of remarks 

before N. York Acad. Med., Feb. 20] <Ibidem, p. 434. [Wa, Win.] 
Grassi, Giovanni Battista. [Prof, ord., Anat. comp. ; Direttore, Gab. Anat. 

coinp., Univ. Roma.] 
1879 n. — Dei protozoi parassiti e specialmente di quelli che sono nell' uomo 

<Gazz. med. ital. lomb., Milano, v. 39, 8. s., v. 1 (45), 8 nov., pp. 445-448. 

1881. — Contribuzione alio studio delle amibe <R. 1st. Lomb. di sc. e lett. 

Rendic, 2. s., v. 14, pp. 353-356. [Wc] 
1882 a. — Intorno ad alcnni protisti endoparassitici ed appartenenti alle 

classi dei flagellati, lobosi, sporozoi e ciliati. Memoria di parassitologia 

comparata <Atti Soc. ital. di sc. nat, Milano, v. 24 (2-3), feb., pp. 135- 

224, pis. 1-4. [Ws.] 
18SS b. — Morfologia e sistematica di alcuni protozoi parassiti. Nota pre- 

liminare <Atti r. Accad. d. Lincei, Roma. Rendic, an. 285, 4. s., v. 4, 

1. semestre (1), 8 genua io, pp. 5-12. [Ws.] 
1888 e. — Significato patologico dei protozoi parassiti dell' uomo. (Questa 

nota forma quasi un'appendice alia mia precedente) <Ibidem (2), 22 

gennaio, pp. 83-89. [Ws.] 
Greig, E. D. W. [Major] ; & Wells, R. T. [Capt.]. 

1911. — An enquiry on dysentery and liver abscess in Bombay <Scient. 

Mem. Off. Med. & San. Dept. Govt. India, Calcutta, n. s. (47), pp. 1-78, 

charts 1-12, 1 diagram, tables 1-3, 3 pis., 32 figs. [Wa, Wm.] 
Grimm, F[erdinand]. [Dr., Berlin.] 

1894 a. — Ueber einen Leberabscess und einen Lungenabscess mit Protozoen 

<Arch. f. klin. Chir., Berl., v. 48 (2), pp. 478-482, pi. 7, figs. 1-12. [Wm.] 
Gros, G. [Dr., Moscou.] 

1849 a. — Fragments d'helminthologie et de physiologie miscroscopique <Bull. 

Soc. imp. d. nat. de Moscou, v. 22 (2), pp. 549-573, pis. 5-6. [Wc] 
Gross, Alfred. [Dr., Oberarzt d. Klinik.] 

1903. — Beobachtungen fiber Amobenenteritis <Deutsches Arch. f. klin. Med., 

Leipz., v. 76 (4-5), IS. Juni, pp. 429^49, pis. 16-17, figs. l-6b. [Wm.] 

Grosse-Allermann, Wilhelm. [Elberfeld.] 

1909. — Studien fiber Amoeba terricola Greeff <Arch. f. Protistenk., Jena, v. 
17 (2), pp. 203-257, figs. A-M, pis. 11-13, figs. 1-27. [Wa, Wm.] 

Gruber, Karl. [Dr.] 

1911. — Ueber eigenartige Korperformen von Amoeba proteus <Arch. f. 
Protistenk., Jena, v. 23 (3), pp. 253-261, figs. 1-1 [Wa, Wm.] 

Guiart, J. [Prof., Faculto de med., Lyon.] 

1910.— PnVis de parasitologic [xii] + 628 pp., 549 figs. 12°. Paris. 


Guiart, J. — Continued. 

TOIL — Peeudo-parasitisme des infnsoires dans I'inteatin de 1'hoinme. [Read 
before Soc. med. d. hop. de Lyon, 7 fev.] <Lyon med., an. 43, v. 116 (19). 
7 mai, pp. 849-853, figs. 1-10. [Wm.] 
de Haan, J.; & Kiewiet de Jonge, G. W. 

1903. — Aanteekeuingen over tropische dysenterie <Geneesk. Tijdsclir. v. 
Nederl.-Indie, batav., Deel 43 (3), pp. 313-330, charts. I Wc. ] 
Hadley, F. A. [Sheffield.] 

1908. — [Tropical abscess of liver.] [Abstract of discussion before 76. Ann. 
Meet. Brit. Med. Ass., Sheffield, July] <Brit. M. J., Loud. (2495), v. 2. 
Oct. 24, p. 1254. [Wa, Wm.] 
Hadley, Philip B. ; & Amison, Elizabeth E. 

1911. — Further studies on blackhead in turkeys < Centra lbl. f. Bakteriol. 
[etc.], Jena, 1. Abt. v. 58 (1), 6. Miirz, Orig., pp. 34^1. [Wa, Wm.] 
Hanes, Granville S. [M. D., Prof., Dis. Rectum, Med. Dept, Univ. Louisville.] 
1909. — Amebic dysentery. A preliminary note based on clinical and patho- 
logical studies <J. Am. M. Ass., Chicago, v. 52 (25), June 19, pp. 1990- 
1992. [Wa, Wm, Wc] 
1909. — Treatment of chronic amebic dysentery. [Remarks before Ky. State 
Med. Ass., Louisville, Oct. 19-21] <Proctologist, St. Louis, v. 3 (4), Dec, 
pp. 257-258. rWm.] 
1910. — Treatment of chronic amebic dysentery. [Read before Ky. State 
Med. Ass., Louisville, Oct. 19-21] <Kentucky M. J., Bowling Green, v. 8 
(1), Jan. 1, pp. 1140-1146, figs. 1-3; discussion, pp. 1147-1149. [Wm.] 
1910. — A case of dysentery with demonstration of motile Ameba on the 
screen. (Presentation of patient) < Ibidem (10), June 15, pp. 1639-1641; 
discussion, p. 1641. [Wm.] 
Hara, S. [Asst.-Arzt, Dr. med.] 

1910. — Bietriige zur Kenntnis der Amoben-Dysenterie <Frankf. Ztschr. f. 
Path., Wiesb., v. 4 (3), pp. 329-371, figs. 1-2, pis. 21-23, figs. 1-6. [MS. 
dated Dec. 190S.] [Wm.] 
Hare, Hobart A. [Dr., Philadelphia, Pa.] 

1909.— [Discussion of Simon, Sidney K., 1909, pp. 1526-1529] <J. Am. M. 
Ass., Chicago, v. 53 (19), Nov. 6, p. 1530. [Wa, Wm, Wc] 
Harold, John. [Med. Registrar, Charing Cross Hosp.] 

1892 a. — Case of dysentery with Amoeba coli in the stools <Brit. M. J., 
Lond. (1670), v. 2, Dec. 31, p. 1429. [Wa, Wm.] 

Harris, H[enry] F. [M. D., Atlanta, Ga.] 

1892 a. — Three cases of amebic dysentery <Med. News, Phila. (103S), v. 

61 (23), Dec. 3, pp. 631-632. [Wa, Wm.] 
1894 a. — Some observations on a method of multiplication of the Amoeba 

dysenteriae (Amoeba coli) <Med. News, Phila. (1141), v. 65 (21), Nov. 

24, pp. 567-569, figs. 1-3. [Wm.] 
1898 a. — Amoebic dysentery. [Read before Nashville Acad. Med.] <Am. 

J. M. Sc, Phila., n. s. (312), v. 115 (4), Apr., pp. 3S4-413, figs. 1-2, 4-5, 

1 pi. [Wm.] 
1901 a. — On the alterations produced in the large intestines of dogs by the 

Amoeba, coli, by heat, and by various chemic substances, with notes on 

the anatomy and histology of the viscus. A research carried on under 

the auspices of Nathan L. Hatfield Prize Committee of the College of 

Physicians and Surgeons of Philadelphia, xviii+19-143 pp., 14 pis. 8°. 

Philadelphia. [Wm.] 

66692— vol 2, pt 1—13 15 


Harris, H[enry] F. — Continued. 

1901. — Experimental dysentery in dogs, with exhibitions of microscopic 

specimens <Proc. Path. Soc, Phila., o. s., v. 22, n. s., v. 4 (8), June 1, 

pp. 191-194 ; discussion, pp. 194-196. [Win.] 
1901. — Experimentell bei Hunden erzeugte Dysenteric [Transl. by C. 

Davidsohn] <Arch. f. path. Anat. [etc.], Berl., v. 166, 16. F., v. 6 (1), 

11. Oct., pp. 67-77. [Wa, Wm.] 
1903 a. — Pathology and clinical history of amebic dysentery. [Read at 54. 

Ann. Sess. Am. Med. Ass.] <J. Am. M. Ass., Chicago, v. 41 (8), Aug. 22, 

pp. 476-480. [Wa, Wm, Wc] 

Hart, Thomas. 

1903 a. — The preparation of permanent stained specimens of Amoeba coli 
<J. Trop. M., Lond., v. 6 (24), Dec. 15, p. 380. [Wa, Wm.] 
Hartmann, Max. [Dr., K. Inst. f. Infektionskrankh., Berlin.] 

1907. — Das System der Protozoen. Zugleich vorlaufige Mitteilung iiber 
Proteosoma [Labbe] <Arch. f. Protistenk., Jena, v. 10 (1), pp. 139-158, 
figs. A-C. [Wa, Wm.] 

1908. — Eine neue Dysenterieamobe, Entamoeba tetragena (Viereck) syn. 
Entamoeba africana (Hartmann). [Read before Deutsch. tropenmed. 
Gesellsch. in Hamburg, 15. Apr.] <Beiheft. z. Arch. f. Schiffs- u. Tropen- 
Hgy., Leipz., v. 12 (5), Aug., pp. 117-127 [pp. 217-227]. [Wm.] 

1909. — Untersuchnngen iiber parasitische Amoben. 1. Entamoeba histoly- 
tica Schaudinn <Arch. f. Protistenk., Jena, v. 18 (2), pp. 207-220, pi. 13, 
figs. 1-25. [Wa, Wm.] 

1909. — Polyenergide Kerne. Studien fiber multiple Kernteilungen genera- 
tive Chromidien bei Protozoen. [Read before Gesellsch. naturf. Fr. in 
Berl., 9. Marz] <Biol. Centralbl., Leipz., v. 29 (15), 1. Aug., pp. 481-187, 
figs. 1-2; (16), 15. Aug., pp. 491-506, figs. 3-12. [Wa.] 

1910. — Nova ameba intestinal, Entamoeba testudinis n. sp. [Portuguese 
and German text] <Mem. Inst. Oswaldo Cruz, Rio de Janeiro-Man- 
guinhos, v. 2 (1), abril, pp. 3-10, pi. 1, figs. 1-9. [MS. dated Nov. 1909.] 

1911. — Die Konstitution der Protistenkerne und ihre Bedeutung fur die 
Zellenlehre. iv pp., 1 p. 1., 54 pp., 13 figs. 8°. Jena. [Wa.] 

1911. — Die Dysenterie-Anioben <Handb. d. path. Protozoen (v. Prowazek), 
Leipz., 1. Lief., pp. 50-66, figs. 1-36, pi. 1, figs. 1-6. [Wa.] 

1912. — Untersuohungen fiber parasitische Amoben. 2. Entamoeba tetra- 
gena Viereck <Arch. f. Protistenk., Jena, v. 24 (3), pp. 163-181, figs. 
A-D, pis. 15-16, figs. 1-46. [Wa, Wm.] 
Hartmann, Max; & Chagas, Carlos [Dr.]. 

1910. — Estudos sobre flajelados. [Portuguese & German text] <Mem. 
Inst. Oswaldo Cruz, Rio de Janeiro-Manguinhos, v. 2 (1), abril, pp. 
64-125, figs., pis. 4-9, figs. 1-91. [Wa.] 

1910. — Sobre a divizao nuclear da Amoeba hyalina Dang. [Portuguese & 
German text] <Mem. Inst. Oswaldo Cruz, Rio de Janeiro-Manguinhos, 
v. 2 (2), pp. 159-167, pi. 10, figs. 1-17. [MS. dated Nov. 1909.] [Wa.] 

Hartmann, Max ; & Naegler, K. 

1908. — Copulation bei Amoeba diploidea n. sp. mit Selbstandigbleiben der 
Gametenkerne wahrend des ganzen Lebenszyklus. [Read 5. Mai] <Sit- 
zungsb. d. Gesellsch. naturf. Fr. zu Berl. (5), 12. Mai, pp. 112-125, pis. 
5-6, figs. 1-15; Vorbemerkung by Hartmann, pp. 112-113. [Wa.] 


Ilartmann, Max; & von Prowazek, 81 

1907. — Blepharoplast, CaryoBom mid Centrosom. Ein Beitrag zur Lehre 
von der Doppelkemigkeit der Zelle <Arch. f. Protistenk., Jena, v. 10 
(2-3), pp. 306-335, figs. 1-8 [Wa, Win I 
Hartmann, Max; & Whitmore, ESugeo K. 

1912. — Untersucliungen iiber parasitische Amoben. 3. Entamoeba coli Lusch 
em. Schawl inn <Arch. f. Protistenk., Jena, v. 24 (3), pp. 182-194, figs. 
A-B, pis. 17-18, figs. 1-29. IWa, Wm.] 
Hartsock, Frederick M. [M. D., U. S. Army.] 

1904 a. — The dysentery of the tropics, with special reference to our insular 
possessions < N. York M. J. [etc.] (1337), v. 80 (3), July 16, pp. 107-109. 
[Wa, Wm, Wa] 
Ilarvie, J. B. [M. D.] ; & Carey, H. W. [M. D.]. 

1911. — A rapidly fatal case of amoebiasis with abscess of the liver originat- 
ing in the village of Green Island, New York <N. York M. J. [etc.] 
(1677), v. 93 (3), Jan. 21, pp. 127-128. [Wa, Wm.] 
Harz, Karl Otto. [Dr. phil. ; Prof., Botan., k. tieriirztl. Hochschule, Munchen.] 
1885 a. — Amoba coli Losch <Encycl. d. ges. Thierh. u. Thierzucht (Koch), 
Wien & Leipz., v. 1, p. 146. [Wa.] 
Hassall, Albert. [M. R. C. V. S. ; Asst. Zool., Bureau Animal Indust, U. S. Dept. 
Agriculture, Washington, D. C] 
1896 b. — Check list of the animal parasites of turkeys (Meleagris gallopavo 
mexicana) <Circular 12, Bureau Animal Indust., U. S. Dept. Agric, 
Wash., 3 pp. [Wa.] 
Hassler [Dr., Med.-major, l re classe] ; & Boisson [Dr., M£d.-major, 2 e classe]. 
1896. — Etude sur les abces dysenteriques du foie <Rev. de m§d., Par., v. 16 
(10), 10 oct, pp. 785-798. [Wm.] 
Head, George Douglas; & Ulrich, Henry L. 

1904. — Some notes on a case of chronic dysentery with Amebae coli in the 
stools <Northwest. Lancet, Minneapolis, v. 24 (13), July 1, pp. 249-250. 
Hehir, Patrick. [Surg.-Capt ; Lecturer, Path. & Clin. Med.. Hyderabad Med. 
1892 b. — The Amoeba coli; its relations to dysentery and tropical suppura- 
tive hepatitis <Indian M. Gaz., Calcutta, v. 27 (11), Nov., pp. 321-323, 
Heiser. [Dr.] 

1910.— [Discussion of Bowman, 1910, p. 846] <Med. Rec N. Y. (2062), 
v. 77 (20), May 14, p. 846. [Wa, Wm.] 
Hektoen, Ludvig. [M. D., Prof., Path., Rush Med. College, Chicago, 111.] 

1892 a. — A case of amoebic dysentery <N. Am. Pract, Chicago, v. 4 (12), 

Dec., pp. 554-560, figs. 1-5. [Wm.] 
1892 b.— Idem <Chicago M. Recorder, v. 3 (8), Oct., pp. 649-654. [Wm.] 
Henderson, Edward. [M. D., Edinburgh.] 

1902 a. — [Discussion on dysentery] <Brit. M. J., Lond. (2177), v. 2, Sept. 
20, pp. 851-852. [Wa, Wm.] 
Herrick, A. B. [M. D., Chief, Surg. Clin., Ancon Hosp.] 

1909. — The surgical treatment of very severe and late cases of amebic 
dysentery. [Read before Canal Zone Med. Soc, Aug.] <Med. Rec., N. Y. 
(2036), v. 76 (20), Nov. 13, pp. 810-812. [Wa, Wm.] 
Herrick, W. W. [M. D., New York.] 

1910. — Pernicious anemia mistaken for amebic ulcerative colitis. With 
observations on the ipecac treatment <Arch. Int. Med., Chicago, v. 6 (6), 
Dec. 15, pp. 662-665 [Wm.] 



1906.— [Discussion of Juergens, 1906, pp. 1607-1608] <Berl. klin. Wchnschr., 
v. 43 (50), 10. Dec, p. 1608. [Wa, Wm.] 
Hickson, S. J. [Prof., F. R. S.] 

1909. — The lobosa <Treatise on Zool. (Lankester), Lond., pt. 1, Introduc- 
tion & Protozoa (1), pp. 68-93, figs.. 1-21. [Wa.] 

Hirschfeld, Ludwig. [Asst., Inst.] 

1909. — Ein Versuch einige Lebcnserscheinungen der Amoben physikalisch- 

chemisch zu erklaren <Ztschr. f. allg. Physiol., Jena, v. 9 (3-4), pp. 

529-534. [Wm.] 
Holt, John Milton. [Phil. B., M. D. ; Passed Asst. Surg., U. S. Pub. Health & 

Mar.-Hosp. Serv.] 
1907. — Amoebic dysentery (chronic), a surgical disease <N. York M. J. 

(1511), v. 86 (20), Nov. 16, pp. 920-923. [Wa, Wm.] 
1907. — Amebic dysentery (chronic), a surgical disease <Mil. Surg., Carlisle, 

Pa., v. 21 (6), Dec. pp. 517-526. [Wm.] 
1908. — Medical versus surgical treatment of amebic dysentery <J. Am. M. 

Ass., Chicago, v. 51 (25), Dec. 19, pp. 2140-2143. [Wa, Wm, Wc] 
1909. — Medical versus surgical treatment of amoebic dysentery <Mil. Surg., 

Richmond, Va., v. 24 (1), Jan., pp. 39^9. [Wm.] 
Hooton, A. [Major I. M. S. ; Agency Surg., Kathiawar.] 

1908. — The treatment of abscess of the liver by aspiration and injection of 

quinine. [Read before 76. Ann. Meet. Brit. Med. Ass., Sheffield, July] 

<Brit. M. J., Lond. (2495), v. 2, Oct. 24, pp. 1251-1252. [Wa, Wm.] 

Hoppe-Seyler, G. [Kiel.] 

1901. — Dysenterie und Amobenenteritis < Deutsche Klinik, Berl. & Wien, v. 

2, Infectionskr., Lief. 36-38, pp. 133-168, figs. 8-12. [Wm.] 
1904 a. — Ueber Erkrankung des Wurmfortsatzes bei chronischer Amoben- 
enteritis. [Read before Physiol. Ver., Kiel] <Miinchen. med. Wchnschr., 
v. 51 (15), 12. Apr., pp. 646-649, 1 fig. [Wa, Wm.] 
Howard, William Travis (jr.). [M. D., Prof., Path., Western Reserve Univ., 
Cleveland, Ohio.] 
1892 a. — The Ameba coli: Its importance in diagnosis and prognosis. With 
the report of two cases. [Read at Semi-Ann. Meet. Med. & Chir. Faculty 
Maryland, Easton, Nov. 15] <Med. News, Phila. (1041), v. 61 (26), Dec. 
24, pp. 705-710. [Wa, Wm.] 
Hoyt, R. E. [Passed Asst. Surg., U. S. Navy.] 

1908. — Result of three hundred examinations of feces with reference to the 
presence of amebae <U. S. Naval Med. Bull., Wash., v. 2 (3), July, pp. 
25-29. [Wa, Wm.] 
1908. — Idem. [Read before 15. Ann. Meet. Philippine Islands Med. Ass., 
Manila, Feb. 27] <Philippine J. Sc, Manila, v. 3 (5), Nov., pp. 417-420. 
Huber. [Dr.; Direktor, inn. Abt, Aug. Viktoria-Krankenhauses, Schoneberg.] 
1909. — Untersuchungen fiber Amobendysenterie <Ztschr. f. klin. Med., Berl., 
v. 67 (4), pp. 262-271, pi. 3, figs. 1-9. [Wm.] 
Huber, J[oh] Ch[ristopher]. [Med.-Rath, Dr. Memmingen.] 

1903 b. — Dysenterieamoben. [Address before Ver. f. inn. Med., Berlin, 13. 
Juli] <Deutsche med. Wchnschr., Leipz., v. 29 (34), 20. Aug., Yer.- 
Beilage, p. 267; discussion, pp. 267-268. [Wa, Wm.] 
1906.— Discussion of Juergens, 1906, pp. 1607-1608] <Berl. klin. Wchnschr., 
v. 43 (50), 10. Dec, p. 1609. [Wa, Wm.] 


Ijinia, Isao. [Ph. D., Prof., Zool., College Sc., Imp. Univ., Japan.] 

1889 b. — [The animal parasites of man.] [Japanese text.] 7+11+400+6 

pp., 7 pis. 8°. Tokio. [Win.] 
1898 a. — On a new rhizopod parasite of man (Amoeba uiiurai n. sp.) 
<Annot. zool. japon., Tokyo, v. 2 (3), pp. 85-94, figs. 1-9. [MS. dated 
Aug. 81.] [Published Oct. 10.] [Wa.] 
Irwin, J. W. [Dr.] 

1903.— [Discussion of Young, G. B., 1903, pp. 241-248] <Am. Pract. & News, 
Louisville, v. 35 (7-8), Apr. 1 & 15, pp. 288-290. [Win.] 
Isbister, J. L. T. [M. B., Adel, Sydney.] 

1899. — Pathological notes upon the above case of amoebic abscess of liver 
and lung. [See Fiaschi, Thomas, 1899, pp. 109-110] < Indian M. Rec, 
Calcutta, v. 1G (4), Jan. 25, pp. 110-111. [Wm.] 
Jacob, O. [Med.-major de l'armee; Prof, au Val-de-Graee,.] 

1911. — Des abces amibiens du cerveau observes au cours de l'hepatite sup- 
purge dysenterique <llev. de chir., Par., an 31, v. 44 (10), 10 oct, pp. 
548-579, figs. 1-5. [Wm.] 
(1911). — Deux cas d'abces du cerveau d'origine amibienne consecutifs a 
des abces du foie dysenteriques <Bull. et inem. Soc. de chir. de Par., n. s., 
v. 37, pp. 119-134. 
Jaeger, H. [Prof., Dr., Konigsberg i. Pr.] 

1901 a. — Ueber Amobenbefunde bei epidemischer Dysenterie <Berl. klin. 
Wchnschr., v. 38 (36), 9. Sept., pp. 917-919. [Wa, Wm.] 

1902 c. — Untersuchungen iiber Amobendysenterie in Ostpreussen. [Read 
before Yer. f. wissensch. Heilk., Konigsberg, 5. Mai] <Deutsche med. 
Wchnschr., Leipz., v. 28 (27), 3. Juli, Ver.-Beilage, pp. 208-210. [Wa, 

(1902 d).— Idem [?] <Verhandl. d. Ver. f. wissensch. Heilk., Konigsb. i. 

Pr. (1), pp. 51-56. 
1902 e. — Erwidernng auf die Bemerkungen Shiga's iiber meine Amobenbe- 
funde bei der in Ostpreussen herrschenden Ruhr <Centralbl. f. Bakteriol. 

[etc.], Jena, 1. Abt, v. 32 (12), 29. Nov., Orig., pp. S65-867. [Wa, Wm.] 
1902 g. — Die in Ostpreussen heimische Ruhr eine Amobendysenterie <Cen- 

tralbl. f. Bakteriol. [etc.], Jena, 1. Abt., v. 31.(12), 14. Mai, Orig., pp. 

551-558, pis. 1-3. [Wa, Wm.] 
1902. — Die in Ostpreussen heimische Ruhr eine Amobendysenterie (mit 

Demonstration der Priiparate an Lichtbildern). [Discussion only] 

<Verhandl. d. Gesellsch. deutsch. Naturf. u. Arzte, Leipz. (73. Versamml. 

zu Hamb., 22.-28. Sept. 1901), 2. Theil, 2. Halfte. med. Abt., pp. 56&-570. 

von Jaksch, Rudolf (Ritter von Wartenhorst). 

1888 a. — Ueber das Yorkommen von thierischen Parasiten in den Faeces der 

Kinder <Wien. klin. Wchnschr., v. 1 (25), 20. Sept., pp. 511-513, 1 fig. 

1896a. — Klinische Diagnostik innerer Krankheiten mittels bakteriologischer, 

chemischer und mikroskopischer Untersuchungsmethoden. 4. vermehrte 

und verbesserte Aufl. xxviii+568 pp., 150 figs. 8°. Wien & Liepzig. 

von Janicki, Constantino. [Dr.] 

1908. — Contribuzione alia conoscenza di alcuni protozoi parassiti della 

Pcriplaneta orientalis (Lophomonas blattarum Stein, L. striata Biitschli. 

Amoeba blattae Biitschli) <Atti r. Accad. d. Lincei, Roma. Rendic, cl. 

di sc. fis., mat. e nat., an. 305, 5. s., v. 17, 2. semestre (3), 2 agosto, pp. 

140-151. [Wa, Wc] 


von Janicki, Constantino — Continued. 

1909. — Ueber Kern und Kernteilung bei Entamoeba blattae Biitschli <Biol. 
Centralbl., Leipz., v. 29 (12), 15. Jimi, pp. 381-393, figs. l-7b. [Wa.] 
Janowski, Wladyslaw. [Dr. med.] 

1897 c. — Zur Aetiologie der Dysenterie < Centralbl. f. Bakteriol. [etc.], 
. Jena, 1. Abt, v. 21 (3), 30. Jan., pp. 88-100; (4), 6. Feb., pp. 151-158; 

(5), 15. Feb., pp. 194-202; (6-7), 5. Marz, pp. 234-255. [Wa, Wm.] 
Jay, Frank Webster. [M. D., Chicago, 111.] 

1S99 a. — Amebic dysentery of army origin <Medicine, Detroit, v. 5 (2), 
Feb., pp. 106-114. [Wm.] 
Jefferis, D. W. [Dr.] 

1910. — [Treatment of dysentery.] [Abstract of discussion before Delaware 
Co. Med. Soc, Chester, Pa., Feb. 24] <Penn. M. J., Athens, v. 13 (7), 
Apr., p. 574. [Wm.] 
Jeffries. [Dr.] 

1904 a. — Presentation of a specimen of urine containing Amoebae. [Secre- 
tary's abstract of paper read before N. York Path. Soc, Feb. 10] <Med. 

Rec, N. Y. (1764), v. 66 (9), Aug. 27, p. 356; discussion, p. 356. [Wa, 

Jelks, John L. [M. D., Memphis, Tenn.] 

1902. — Three months' office experience in the treatment of chronic dysen- 
tery. [Read before Miss. Valley Med. Ass., Kansas City, Mo., Oct. 17] 
<Memphis M. Month., v. 22 (12), Dec, pp. 630-641. [Wm.] 

1905.— [Discussion of Turtle, James P., 1905, pp. 348-353] < Lancet-Clinic, 
Cincin., v. 94. n. s., v. 55, Sept. 23, pp. 353^354. [Wm.] 

(1908). — Amebiasis <Memphis M. Month., Sept. 

1909.— Amebiasis : Its symptomatology, diagnosis, sequelae, and the use of 
formalin and copper phenol sulphonate in the treatment. [Read before 
Am. Proctol. Soc, Chicago, June 1, 190S] <J Tenn. State M. Ass., Nash- 
ville, v. 1 (9), Feb., pp. 18-20. [Wm.] 

1909. — Appendicostomy as an aid to the treatment of malignant and intract- 
able dysentery <Proctologist, St. Louis, v. 3 (3). Sept.. pp. 233-235. 

1910. — Amebiasis, complicated in one instance by pellagra; in [an]other by 
eighteen adenomata. [Remarks before Tenn. State Med. Ass.. Apr. 12-14] 
<Ibidem, v. 4 (2), June, p. 55. [Wm.] 

1910. — Amebiasis. Complicated in one instance by pellagra; case report — 
presentation of patient; in another by eighteen adenomata <J. Tenn. M. 
Ass., Nashville, v. 3 (4), Aug., pp. 94-97; discussion, pp. 97-102. [Wm.] 

1910. — Skin manifestations of amebiasis <Tr. Am. Proctol. Soc. [St. Louis], 
(12. Ann. Meet., June 6-7), pp. 128-131; discussion, pp. 131-132. [Wm.] 

1910. — Idem < Proctologist, St. Louis, v. 4 (3), Sept., pp. 202-205: discus- 
sion, pp. 205-206. [Wm.] 
Jennings, E. [Major, I. M. S. ; Supt, Central Prison, Bareilly.] 

1905. — Dysentery as it occurs in jails with regard to etiology, prophylaxis 
and treatment < Indian. M. Gaz., Calcutta, v. 40 (7), July. pp. 247-250. 
Jennings, Herbert S. [Ph. D. ; Instructor, Zool., Univ. Mich., Ann Arbor, Mich.] 

1905. — The movements of Amoeba. [Secretary's abstract of paper read 
before Soc. Normal & Path. Physiol., Univ. Penn., Nov. 21, 1904] <Univ. 
Penn. M. Bull., Phila., v. 17 (12), Feb., p. 416. [Wa, Wc] 
Jensen, Vilhelm [Peter Herlof]. 

1898 a. Oui dyrknlng af am0ber <Hosp.-Tid., Kj0benh., 41. Aarg.. 4. R., 
v. 6 (6), 9. Feb., pp. 133-142: (7), 16. Feb., pp 165-170. [Wm.] 


Jensen, Vilhelm [Peter Herlof] — Continued. 

1898 c. — Demonstration af forskellige Am0bekulturer< Ibidem (29), 20. 
Juli, pp. 767-768. [Wm.] 

Jermain, L. F. [M. D., Milwaukee, Wis.] 

1899 a. — Amoebic abscess of liver, with report of a case < Milwaukee M. J., 
v. 7 (12), Dec, pp. 406-409. [Wm.] 

Johnson. [Dr.] 

1908.— [Discussion of Killough, J. N., 1908, pp. 371-377] <Tr. M. Ass. Ala- 
bama, Montgomery (Apr. 21-24), pp. 377-378. [Wm.] 
Juergens, Rudfolf Joh.]. [Dr., Oberarzt, Berlin.] 

1892 a. — [Einwanderung von Amoben in die Harnblase] <Deutsche med. 
Wchnschr., Leipz. & Berl.,. v. 18 (20), 19. Mai, pp. 454-455. [Wa, Wm.] 

1902. — Zur Kenntniss der Darm-Amoben und der Amoben-Enteritis <Verof- 

fentl. a. d. Geb. d. Mil.-San.-Wes., Berl., Heft 20, pp. 110-160, pis. 1-8, 

figs. 1-21. [Wm.] 
1903. — Zur Aetiologie der Ruhr <Deutsche med. Wchnschr., Leipz., v. 29 

(40), 12. Nov., pp. 841-843. [Wa, Wm.] 
1906. — Ueber Amoben-Enteritis und ihre Beziehungen zur epidemischen 

Ruhr. [Secretary's abstract of paper read before Gesellsch. d. CharitG- 

Aerzte, 1. Nov.] <Berl. klin. Wchnschr., v. 43 (50), 10. Dec., pp. 1607- 

1608; discussion, pp. 1608-1609. [Wa, Wm.] 
1907. — Amoeben-enteritis. [Abstract of remarks, with demonstration, before 

Gesellsch. d. Charit6arzte, Berl., 1. Nov., 1906, by Fleischmann] <Deutsche 

med. Wchnschr., Leipz., v. 33 (6), 7. Feb., p. 245; discussion, pp. 245-246. 

[Wa, Wm.] 
1907. — Die Amoben-Enteritis und ihre Beziehungen zur Dysenterie <Ztschr. 

f. exper. Path. u. Therap., Berl., v. 4 (3), 21. Dec, pp. 769-816, pis. 24-27, 

tigs. 1-16. [Wa.] 
Kaestner, Paul. [Tierarzt, Berlin.] 

1906. — Die tierpathogenen Protozoen. vii+161 pp., 42 figs. 8°. Berlin. 

Kartulis, Stephan. [Surg., Govt. Hosp., Alexandria, Egypt.] 

1885c — Ueber Riesen-Amoben (?) bei chronischer Darmentzundung der 

Aegypter <Arch. f. path. Anat. [etc], Berl., v. 99, 9. F., v. 9 (1), 2. Jan., 

pp. 145-147, pi. 4, fig. 5. [Wa, Wm.] 

1886 a. — Zur Aetiologie der Dysenterie in Aegypten <Ibidem, v. 105, 10. F., 
v. 5 (3), Sept., pp. 521-531, pi. 17, figs. 1-3. [Wa, Wm.] 

1887 b. — Zur Aetiologie der Leberabscesse. Lebende Dysenterie- Amoben im 
Eiter der dysenterischen Leberabscesse <Centralbl. f. Bakteriol. [etc], 
Jena, 1. J., v. 2 (25), pp. 745-748. [MS. dated 20. Nov.] [Wa, Wm, Wc] 

1889 a. — Ueber tropische Leberabscesse und ihre Verhaltnisse zur Dysen- 
terie <Arch. f. path. Anat. [etc.], Berl., v. 118, 11. F., v. 8 (1), 1. Oct., 
pp. 97-121, pi. 7, figs. 1-3. [Wa, Wm.] 

1890 b. — Ueber weitere Verbreitungsgebiete der Dysenterie-Amoben <Cen- 
tralbl. f. Bakteriol. [etc], Jena, v. 7 (2), 4. Jan., pp. 54-55. [MS. dated 
Nov. 1889.] [Wa, Wm, Wc] 

1891 a. — Einiges fiber die Pathogenese der Dysenterieamoben < Ibidem, v. 9 
(11), 21. Marz, pp. 365-372. [MS. dated Jan.] [Wa, Wm, Wc] 

1893 a. — Ueber pathogene Protozoen bei dem Menschen. 1. Gregarinose der 
Leber und der Bauchmuskeln. 2. Amoben bei Knochennekrose (Osteo- 
myelitis) des Unterkiefers <Ztschr. f. Hyg. u. Infectionskrankh., Leipz., 
v. 13, pp. 1-14, 12 figs., pis. 1-2. [Wa, Wm.] 

1896 a. — Dysenterie (Ruhr) <Spec Path. u. Therap. . . . Nothnagel, Wien, 
v. 5, 1. Halfte, 3. Theil, pp. 1-95. [Wm.] 


Kartulis, Stephan — Continued. 

1903 a. — [Dysenterie Egyptens.] [Secretary's abstract of paper read before 
1. Egypt, med. Cong., 19.-23. Dec. 1902] <Deutsche med. Wchnschr., 
Leipz., v. 29 (4), 22. Jan., Ver.-Beilage, p. 31. [Wa, Win.] 

1903 b. — [Etiology and treatment of tropical dysentery.] [Secretary's ab- 
stract of paper read before 1. Egypt, med. Cong., Cairo, Jan. 2] <Med. 
Rec, N. Y. (1681), v. 63 (4), Jan. 24, pp. 142-143. [Wa, Wm.] 

1903 c. — Ueber Amobenosteomyelitis des Unterkiefers. [Abstract of paper 
read before Panhellen. med. Kong, zu Athens, 1901] <Centralbl. f. 
Bakteriol. [etc.], Jena, 1. Abt, v. 33 (15-16), 27. Juni, Ref., pp. 471^72. 
[Wa, Wm.] 

1904 a. — Gehirnabscesse nach dysenterischen Leberabscessen < Ibidem, v. 37 
(4), 12. Dec, Orig., pp. 527-530, 1 pi., figs. 1-2. [Wa, Wm.] 

1904. — Ueber mit Appendicitis complicirte Leberabscesse <Ztschr. f. Hyg. u. 

Infectionskr., Leipz., v. 48 (3), 16. Dec, pp. 499-511, pi. 3, figs. 1-2. [Wa.] 
1906. — Die Amobendysenterie. <Handb. d. path. Mikroorganism., Jena, 1. 

Erganzungsbd. (1), pp. 347-384, figs, a-1, pi. 7. [Wa.] 
Kaupp, Benjamin Franklyn. 

1911. — Entero-hepatitis (amoebiasis) <Am. Vet. Rev., N. Y., v. 39 (4), 

July, pp. 410-416, figs. 1-5. [Wa, Wm.] 
Kelsch, [Louis- Felix-] Achille; & Kiener, Paul-Louis [-Andre]. 

18S9 a. — Traite des maladies des pays chauds, region pretropicale. viii-f- 

908 pp., 36 figs., 6 pis. 8°. Paris. [Wm.] 
Kernig, W. [Dr., Oberarzt, Obuchow-Frauen-Hosp.] ; & Ucke, A. [Dr., Pro- 
sector, Deutsch. Alexander Hosp. f. Manner]. 
1901 a. — Ueber Amoben-Enteritis in St. Petersburg <St. Petersb. med. 

Wchnschr., v. 26, n. F.. v. 18 (25), 23. Juni (=6. Juli), pp. 299-307. 

Keysselitz, G. 

1908. — Die Entwicklung von Myxobolus pfeifferi Th. 1. Teil <Arch. f. 

Protistenk., Jena, v. 11 (2-3), pp. 252-275, figs. A-G, pis. 13-14, 99 tigs. 

[Wa, Wm.] 
1908.— Studien fiber Protozoen < Ibidem, pp. 334-350, pis. 19-21, 44 figs. 

[Wa, Wm.] 
Klewiet de Jonge, G. W. 

1904 a. — De aetiologie der tropische dysenterie <Geneesk. Tijdschr. v. 

Nederl.-Indie, Batav., Deel 44 (2), pp. 72-91. [Wa] 
Killough, J. N. [M. D., Woodlawn, Ala.] 

1908. — Diagnosis and treatment of amebic dysentery <Tr. M. Ass. Alabama, 

Montgomery (Apr. 21-24), pp. 371-377; discussion, pp. 377-378. [Wm.] 
1909. — Diagnosis and treatment of amebic dysentery < Merck's Arch., N. Y., 

v. 11 (6), June, pp. 174-176. [Wm.] 
King, Howard D. [M. D., Tulane Univ., New Orleans, La.] 

1911. — The epidemiology of amoebiasis in the southern United States, with 

some pertinent remarks as to the absence of liver abscess in the same 

regions <J. Trop, M. & Hyg., Lond., v. 14 (12), June 15, pp. 182-188. 

[Wa, Wm.] 
Kisskalt, Karl [Dr., Privatdoz., Oberasst., Hyg. Inst, Univ. Berlin] ; & Hart- 

mann, Max [Dr., Privatdoz., Zool., Univ. wissensch. Hilfsarb., k. Inst. f. 

Infektionskr., Berlin]. 
1907. — Praktikum dor Bakteriologie und Protozoologie. vi-f-174 pp., 50 

figs. 4°. Jena. [Wa.] 
1910.— Idem. 2. erweiterte Aufl., 2. Teil: Protozoologie. vi+106 pp., 76 

figs. 4°. Jena. [Wa, Wm.] 


Koch, J. A. [Dr., Java.] 

1903 a. — Over tropiseh leverahsces en de chirurgische behandlung <Nederl. 
Tijdschr. v. Geneesk.. Amst, 2. R., v. 89, 2. Afd. (4), 25 Juli, pp. ITS 195; 
(5), 1 Aug., pp. 244-259, 1 fig. [Wm.] 

1904 a.— Ueber tropische Leberabscesse. [Transl. of 1903 a] <Mitt. a. d. 
Grenzgeb. d. Med. n. Chir., Jena, v. 13 (1), pp. 81-112, 1 fig. [Wm.] 

Koch, Robert. [Director, Inst. f. Infectionskr., Berlin.] 

(1883). — Berichte liber die Tiitigkeit d. Expedition z. Erforschung d. 
Cholera in Agypten und Indien <Deutscher Reichsanzeiger. 
Koch, Robert; & Gaffky, Georg. 

1887 a. — Einige in Egypten und Indien gernachte Beobachtungen, verschie- 
dene Krankbeiten (auschl. Cholera) betreffend, nebst den zugehorigen 
Obduktions-Protokollen <Arb. a. d. k. Gsndhtsainte., Berl., v. 3, Anlage 
6, pp. 62-78. [Wm.] 
Koidzumi, M. [Dr.] 

1909. — On a new parasitic Amoeba, Entamoeba nipponica, found in the in- 
testine of Japanese <Centralbl. f. Bakteriol. [etc.], Jena, 1. Abt., v. 51 
(6), 9. Oct., Orig., pp. 650-654, figs. 1-7. [Wa, Wm.] 
Kov&cs, Friedrich. 

1892 a. — Beobachtungen und Versuche iiber die sogenante Amoebendysen- 
terie <Ztschr. f. Heilk., Berl.. v. 13 (6), 1. Dec, pp. 509-551, pi. 15. figs. 
1-6. [Wm.] 

1892 b. — Ueber Amoebendysenterie. [Secretary's abstract of paper read 
before k. k. Gesellsch. d. Aerzte in Wien, 2. Dec] <Wien. med. Presse, 
v. 33 (49), 4. Dec, pp. 1965-1967. [Wm.] 


1906.— [Discussion of Juergens, 1906, pp. 1607-1608] <Berl. klin. 
Wchnschr., v. 43 (50). 10. Dec, p. 1609. [Wa, Wm.] 
Krinitski, S. I. 

1911. — K voprosu o naryvakh pecheni pri amebnol dizenterii'. [Liver ab- 
scesses in amoebic dysentery.] [Russian text] <Russk. Vrach, St. 
Petersb., v. 10 (22), 28 maia. pp. 946-949; (23), 4 lunia. pp. 976-979. 
Krouse, Louis J. [M. D., Cincinnati, Ohio.] 

1910. — A case of amebiasis. [Reported to Acad. Med., Cincinnati, Nov. 29, 
1909] <Lancet-Clinic, Cincin., v. 103 (10), Mar. 5, pp. 269-270. [Wm.] 
Kruse. [Prof.] 

1902. — Der jetzige Stand der Dysenteriefrage < Deutsche Aerzte-Ztg., Berl., 
[v. 4] (2), 15. Jan., pp. 25-30. [Wm.] 
Kruse, Walther; & Pasquale, Allessandro. 

1893 a. — Eine Expedition nach Egypten zum Studium der Dysenterie und 
des Leberabscesses <Deutsche med. Wchnschr., Leipz. & Berl., v. 19 
(15), 13. Apr., p. 354; (16), 20. Apr., pp. 378-379. [Wa, Wm.] 

1894 a. — Untersuchungen fiber Dysenterie und Leberabscess <Ztschr. f. 
Hyg. u. Infectionskrankh., Leipz., v. 16, pp. 1-14S, pis. 1-6. [Wa. Wm.j 

Kruse, W[ilhelm Arthur Karl]. 

1896 a. — Systematik der Protozoen. (In Flugge, C. Die Mikroorganisinen, 
etc 3. Aufl., 2. Theil, 4. Abschnitt, pp. 600-700, 26 figs. 8°. Leipzig.) 
Kubo, N. [Dr.] 

1912. — Die atiologische Bedeutung der Entamoeba histolytica bie Amoben- 
dysenterie nach anatomisch-histologischen Befunden <Arch. f. Schiffs- 
u. Tropen-Hyg., Leipz., v. 16 (21). Nov., pp. 713-721, 1 fig. [Wa, Wm.] 


Kuenen, W. A. [Dr., Medan, Sumatra.] 

1909. — Die Aetiologie und Diagnose der Amoebiasis, nach einem Vortrag, 
gehalten vor der Niederlandischen Gesellschaft fur tropische Medizin zu 
Leiden (Januar 1909) < Janus, Harlem, v. 14 (7), juillet, pp. 542-569; 
(8), aout, pp. 629-643. [Wm.] 

(1909). — Die pathologische Anatomie der Amobiasis, verglichen mit ande- 
ren Formen von Dysenterie <Beihefte (7) z. Arch, f. Schiffs- u. Tropen- 
Hyg., Leipz., v. 13. 

1910.— Idem. [Abstract] <Munchen. med. Wchnschr., v. 57 (28), 12. Juli, 
p. 1515. [Wa, Wm.] 
Kunstler, Joseph. [Prof, adjoint de zool., Univ. de Bordeaux.] 

1888 b. — Sur quelques infusoires nouveaux ou peu connus <Compt. rend. 
Acad. d. sc, Par., v. 107 (24), 10 dec., pp. 953-955. [Wa, Wm, Wc] 
Kurtz, Russell L. [M. D., Neoga, 111.] 

1903. — Report of a case of amebic dysentery in Illinois with special refer- 
ence to " acetozone " treatment. [Read before 56. Ann. Meet. Aesculapian 
Soc. Wabash Valley, Tuscola, 111., May 28] <Med. Fortnightly, St. 
Louis, v. 24 (2), July 25, pp. 535-542. [Wm.] 

1903 a. — A case of amebic dysentery in Illinois, with special reference to 
acetozone treatment <Medicine, Detroit, v. 9 (8), Aug., pp. 595-598. 

Kuschakewitsch, Sergius. [Odessa.] 

1907. — Beobachtungen iiber vegetative, degenerative und germinative Vor- 
gllnge bei den Gregarinen des Mehlwurindarms <Arch. f. Protistenk,, 
Jena, Suppl. 1, Fesfbd. z. 25jahr. Prof.-Jubil. Richard Hertwig, pp. 202- 
249, figs. A-M, pis. 13-16, figs. 1-108. [Wm.] 
Labbe, Alphonse. [Dr.-6s-sc. ; Conservateur des collect, zool., Sorbonne, Paris.] 
1899 a.— Sporozoa. 8°. Berlin. (Das Tierreich, Berl., 5. Lief., xx+180 
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Lafleur, Henri A. 

1890 a. — Demonstration of Amoeba coli in dysentery. [Secretary's abstract] 
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1891 a. — Dysentery ; abscess of liver ; Amoeba coli in stools and sputum ; 
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1895. — [Amoebic abscess of liver.] [Discussion of Finley & Adami, 1895, 
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1897 a.— Amoebic dysentery <Syst. Med. (Allbutt), Lond., v. 2, pp. 753-783. 

1897. — Amoebic abscess of the liver <Ibidem, v. 4, pp. 153-169. [Wm.] 

Lamb, Daniel Smith. [A. M„ M. D., Washington, D. C] 

1907. — Case of amebic dysentery with abscesses of the liver. [Reported 
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Lambl, D. F. [Dr.] 

1860 a.— Aus dein Franz Josef-Kinder-Spitale in Prag. 1. Th. : Beobach- 
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Histologic Nach eigenem und von Prof. Loschner klinisch verwerthetem 
Materia le vergleichend zusarnmengestellt. xiii + 384 pp., 4 figs., 25 pis. 
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1908. — La botryomycose son histogenese — sa nature parasitaire <J. de 

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1863 a. — Die menschlichen Parasiten und die von ihnen herriihrenden 
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Krankheiten. Ein Hand- und Lehrbuch fiir Naturforscher und Aerzte. 
2. Aufl., v. 1, 1. Lief., 1. Abt, viii+336 pp., 130 figs. 8°. Leipzig & Heidel- 
berg. [Wa, Wm.] 

1886 d. — The parasites of man, and the diseases which proceed from them. 
A textbook for students and practitioners. Natural history of parasites 
in general. Systematic account of the parasites infesting man. Pro- 
tozoa — Cestoda. Transl. from the German with the cooperation of the 
author, by William E. Hoyle. xxvi pp., 1 1., 771 pp., 404 figs. 8°. Edin- 
burgh. [Wa. Wm.] 

Levander, Kaarle Mainio. [Dr. phil., o. Prof., Zool., Alex.-Univ., Helsingfors, 
1908. — [Entamoeba buccalis (v. Prowazek).] [Abstract of remarks, 7 dec. 
1907] <Medd. Soc. pro Fauna et Flora Fennica, Helsingfors (1907-08), 
v. 84, pp. 49-50. [Wa.] 

Prison, Charles G. [First Lieut.. Mod. Reserve Corps, U. S. Army.] 

1012. — Bhtero vesical fistula of amebic origin. [Read at 20. Ann. Meet.] 
<Mil. Surg.. Wash., v. .'JO (5), May, pp. 584-589. [Wm.] 


Lewis, Timothy Richards. [M. B., Asst. Surg., Her Majesty's Forces, attached 
to San. Commr., Govt. India.] 
1870 a. — A report on the microscopic objects found in cholera evacuations, 
&c < 6. Ann. Rep. San. Com. India, Calcutta (1869), App. A, pp. 125- 
178, pis. 1-24, 3 maps. [Wm.] 
Lewis, W. Milton. [M. D., Baltimore, Md.] 

L896 a. — A case of amoebic dysentery <Maryland M. J., Bait. (794), v. 35 
(9), June 13, pp. 145-140. [Wm.l 
von Leyden, Ernst; & Loewenthal, Waldemar. 

1905 a. — Entamoeba buccalis Prowazek bei einem Fall von Carcinom des 
Mundbodens <Charite-Ann., Berl., v. 29, pp. 3-11, pi. 1, figs. 1-12. [Wm.] 
Liebetanz, Erwin. [Dr., prakt. Tierarzt, Janowitz i. P.] 

1905 a. — Die parasitische Protozoen des Wiederkauermagens. [Prelimi- 
nary article] <Berl. tieriirztl. Wchnschr. (18), 4. Mai, pp. 313-314. 
[Wa, Wm.] 
(1905).— Idem. [Original.] 84 pp. 8°. Bern. 

1910. — Die parasitischen Protozoen des Wiederkauermagens <Arch. f. 
Protistenk., Jena, v. 19 (1), pp. 19-80, fig. 1, pis. 1-2, figs. 1-58. [MS. 
dated Mai 1905.] [Wa.] 
Lindner, P. 

(1896 a). — Das Vorkommen von Amoben im Garungsbetriebe < Wchnschr. 
f. Brauerei, Berl., p. 1231. 
Liston, W. Glen. [Major I. M. S.] 

1911. — Contributions to the study of pathogenic amoebae from Bombay. 
Part 1. An examination of some cultures of amoebae isolated from 
dysenteric lesions and other sources < Quart. J. Micr. Sc, Lond., n. s. 
(226), v. 57 (2), Nov., pp. 107-122; 127-128, pis. 16-18, figs. 1-32. [MS. 
dated Nov. 1910.] [Wa.] [For pt. 2, see Martin, C. H., 1911, pp. 
Lobas, N. S. 

1894 a. — K kazuistik amoebiikh enteritov. [Occurrence of amebic enteritis.] 
[Russian text] <Vrach, St. Petersb., v. 15 (30), 28 yulia, pp. 845-847. 
Lock wood, Charles E. [M. D., New York.] 

1897 a. — A contribution to the study of amoebic dysentery. [Read Jan. 26] 

<Tr. M. Soc. N. York, Phila., pp. 244-251, 2 figs. [Wm.] 
1897 b.— Idem <Med. Rec, N. Y. (1378), v. 51 (14), Apr. 3, pp. 475-478, 
figs. 1-2. [Wm.] 
Loesch, F. [Klin. Asst. & Privatdocent, Innere Med., St. Petersburg.] 

1875 a. — Massenhafte Entwickelung von Amoeben im Dickdarm <Arch. f. 
path. Anat. [etc.], Berl., v. 65, 6. F., v. 5 (2), 10. Nov.. pp. 196-211, pi. 10. 
figs. 1-3. [Wa, W T m.] 
Loewenthal, Waldemar. 

1903.— [Discussion of Huber, J. Ch., 1903 b] <Deutsche med. Wchnschr., 
Leipz., v. 29 (34), 20. Aug., Ver.-Beilage, pp. 267-268. [W T a, Wm.] 
Loewenthal, Waldemar; & von Rutkowski, Walter. 

1907. — Die Wirkung von Rontgen und Radiumstrahlen auf Trypanosoma 
lewisii <Therap. d. Gegenw., Berl., v. 48, n. F., v. 9 (9), Sept., pp. 393- 
395. [Wm.] 
Long. J. D. [Passed Asst. Surg., U. S. Pub. Health & Mar.-Hosp. Serv.] 

1909.— Amebic dysentery. [Read at 39. Ann. Meet.. State Soc, San Jose, 
Apr.] <Calif. State J. M., San Fran., v. 7 (6), June, pp. 199-201. [Wa.] 
1909.— Idem < Proctologist, St. Louis, v. 3 (2), June, pp. 56-57. [Wm.] 


Long, J. D. — Continued. 

1910.— Amebiasis < Calif. State J, M .. San Fran., v. 8 (2), Feb., pp. 47-49. 
Lorentz, E. [Dr.] 

1911. — Ipecacuanha tegen dysenteric <Med. Weekbl., Ainst, v. 18 (18), 29 
Juli, pp. 225-227. [MS. dated Juni ] [Wm.] 
Low, George Ctarmichael]. 

1912. — [Demonstration of specimens of amoebae sent by Major Marshall 
from Edinburgh] <Tr. Soc. Trop. M. & Hyg., Lond., v. 5 (6), Apr., p. 
227. [Wm.] 
Luehe, Max[imilian Friedrich Ludwigj. [Privatdoc, Zool. & vergl. Anat., zo«l. 
Mas., Konigsberg i. Pr.] 
'906. — Die im Blute schmarotzenden Protozoen und ihre nachsten Ver- 
wandten <Handb. d. TropenkrankL. (Mense), Leipz., v. 3, pp. 69-268, 
figs. 1-60, pis. 6-S. [Wa. Wm] 
009. — Genera tionswechsel bei Protozoen. [Read 16. Nov. 1908] <Schrift. 
d. phys.-okonoin. Gesellsch. zu Konigsb. i. Pr. (1908), v. 49, 10. Mai, pp. 
418-424. [Wa.] 
Lutz, Adolph. [Dr. ; Direktor. bakteriol Inst, Sao Paulo.] 

1891 a. — Zur Kenntniss der Amoben- Enteritis und Hepatitis <Centralbl. f. 
Bakteriol. [etc.], Jena. v. 10 (8). 5. Sept., pp. 241-248. [MS. dated 15. 
Juni.] [Wa, Wm.] 
Lyons, Randolph. [M. D., New Orleans La.] 

1912. — Observations on the effect of ipecac, phenol and salicylic acid on 
amebae in vitro. [Read before Am. Soc. Trop. Med., 1911] <N. Orl. M. 
& S. J., v. 64 (12), June, pp. 881-887. [Wm.] 
1912. — Discussion of Dr. Simon's paper [see Simon, Sidney K., 1912, pp. 373- 
377] <N. Orl. M. & S. J., v. 65 (5), Nov., pp. 377-378. [Wm.] 
MacCallum, William George. [M. D., New York.] 

1906. — Tropische Leberkrankheiten Deutsch von C. Mense <Handb. d. 
Tropenkrankh. (Mense), Leipz., v. 3, pp. 22-68, pis. 4-5. [Wa.] 
McCarrison, Robert. [M. D., M. R. C. P. Lond.; Capt. I. M. S.] 

'909. — Observations on the amoebae in the intestines of persons suffering 
from goitre in Gilgit < Quart, J. Micr. Sc, Lond., n. s. (212), v. 53 (4), 
July, pp. 723-736, figs. 1-24. [MS. dated Mar. 9.] [Wa, Wm.] 
1909-10.- — Observations on the amoebae in the intestines of persons suffer- 
ing from goitre in Gilgit < Collect Papers Lister Inst. Prevent. M., 
Lond. (6), pp. 723-736, figs. 1-24. [MS. dated Mar. 9, 1909.] [Wa.] 
McCulloch, Henry D. [M. B.] 

1906 a. — Amoebic and bacillary dysentery. [Letter to editors, dated July 
23] <Brit. M. J., Lond. (2380) v v. 2 Aug. 11, p. 332. [Wa, Wm.] 
McDill, John R. [M. D., Manila, P. I.] 

1907. — Dysenteric abscess of the liver in the Philippine Islands. [Read be- 
fore 58. Ann. Sess. Am. Med. Ass Atlantic City, N. J., June] <J. Am. 
Iff, Ass., Chicago, v. 49 (6). Aug. 10. pp. 491-493; discussion, p. 493. 
[Wa, Wm.] 
McDilL John R. ; & Musgrave, William E. 

!905a. — Amebic infection of the urinary bladder without recto-vesical 
fistula <Med. News, N. Y.. v. 87 (25), Dec. 16, pp. 1163-1164. [Reported 
Manila Med. Soc, Nov.. 1904] [Wm.] 
Mcfllroj, J. B. [M. D., Stovall, Miss] 

1902. — Amebic dysentery, with report of a case complicated with malaria. 
[Read before Tri-State Med. Ass (Miss., Ark., & Tenn.), Memphis, Nov. 
20, 1901] <Memphis M. Month v. 22 (4), Apr., pp. 169-176. [Wm.] 


Macfadyen. Allan. [M. D. ; Prof., Bacterid., College State Med., London.] 

1893. — Bacteriological notes on a case of tropical abscess of the liver 

<Brit. M. J., Lond. (1698), v. 2, July 15, p. 114. [Wa, Wm.] 
1893. — Further bacteriological notes [to Fayrer, Joseph, 1893, pp. 521-545] 
<Hyg. & Dis. Warm Climates (Davidson), Edinb. & Lond., pp. 531-532. 
MacLeod, Neil. [M. D., Edinburgh.] 

1895. — Tropical abscess, rarely a primary, usually :i secondary, affection of 
the liver < Lancet, Loud. (3765), v. 73, v. 2, Oct. 26, pp. 1037-1039. 
McMillan, Roscoe D. [M. D., Red Springs, N. C] 

1912. — Amebic dysentery. [Read before N. Carolina State Med. Soc, Ilen- 
dersouville, June 18] <01d Dominion J. M. & S., Richmond, v. 16 (2), 
Aug., pp. 47-52. [Wm.] 
McMurtry, Lewis S. [Louisville, Ky.] 

1910.— [Discussion of Hanes, Granville S., 1910, pp. 1140-1146] <Ken- 
tucky M. J., Bowling Green, v. 8 (1), Jan. 1, p. 1147. [Wm.] 
Maggiora, Arnaldo. [Dr.; Prof., Univ. di Torino.] 

1891. — Alcune osservazioni microscopiche e batteriologiche fatte durante 
una epidemia di entero-colite dissenterica. [Read 10 apr.] <Gior. r. 
Accad. di med. di Torino, an. 54 [3. s.], v. 39 (7-8), luglio-agosto, pp. 
718-733. [Wm.] 
1892 a. — Einige mikroskopische und bakteriologische Beobachtungen wahr- 
end einer epidemischen dysenterischen Dickdarmentztindung <Centra!bl. 
f. Bakteriol. [etc.], Jena, v. 11 (6-7), 20. Feb., pp. 173-184. [MS. dated 
Dec. 1891.] [Wa, Wm, Wa] 
Mallory, Frank Burr. [M. D.] 

1897 a. — On certain improvements in histological technique. 1. A differen- 
tial stain for Amoebae coli. 2. Phosphotungstic-acid-haematoxylin stain 
for certain tissue elements. 3. A method of fixation for neuroglia fibres 
<J. Exper. M., N. Y., v. 2 (5), Sept., pp. 529-533, pi. 41, figs. 1-5. [Wa, 

Manaud, A. 

1911. — Traitement de la dysenterie amibienne par la poudre d'ipecac 
deseni6tinisee <Bull. Soc. de path, exot, Par., v. 4 (5), 10 mai, pp. 
322-324; note by Bertrand, p. 325. [MS. dated 20 mars.] [Wa, Wm.] 
Manner, Franz. [Dr.] 

1896 a. — Ein Fall von Amobendysenterie und Leberabscess <Wien. klin. 
Wchnschr., v. 9 (8), 20. Feb., pp. 129-131; (9), 27. Feb., pp. 153-155. 
Manson, (Sir) Patrick. [M. D., M. R. C. P., LL. D. ; Lecturer, Trop. Dis., St. 
George's Hosp. Med. School; and Lond. School Trop. Med.] 
1894. — Remarks on amoebic abscess of the liver. With a report on the 
pathology by James Galloway <Brit. M. J., Lond. (1735), v. 1, Mar. 31, 
pp. 676-678, 1 fig. [Wm.] 
1901 a.— Dysentery <Pract. Med. (Gibson), Phila., v. 1, pp. 261-265. [Wm.] 

1901 b. — Liver abscess of warm climates < Ibidem, pp. 265-270. [Wm.] 

1902 g.— [Discussion on dysentery] <Brit. M. J., Lond. (2177), v. 2, Sept. 
20, p. 851. [Wa, Wm.] 

1904. — Tropical diseases. A manual of the diseases of warm climates. 

xxiv+756 pp., 126 figs., 2 pis. 12°. London. [Wa.] 
1907. — Idem. 4. ed., thoroughly revised and enlarged, xx+876 pp., 241 

figs., 7 pis., frontispiece. 12°. New York. [W T m.] 


Mansoii, (Sir) Patrick — Continued. 

1908. — [Tropical abscess of liver.] [Abstract of discussion before 76. Ann. 
Meet. Brit. Med. Ass., Sheffield, July] <Brit. M. J., Lond. (2495), v. 2, 
Oct. 24, p. 1253. [Wa, Wm.] 

Marcano, G. [Dr.] 

190S. — Sur un travail de . . . concernant le diagnostic des abces dysen- 
teriques de la convexite du foie. [Rapport par A. Chauffard, 5 mai] 
<Bull. Acad, de m§d., Par., 3. s., v. 59 (18), pp. 501-505; discussion, pp. 
505-506. [Wm.] 

Marchoux. Emile. [Dr., l'lnst. Pasteur, Paris.] 

1899 c. — Note sur la dysenterie des pays chauds. [Read 4 nov.] <Compt. 

rend. Soc. de biol., Par., 11. s., v. 1 (32), 10 nov., pp. 870-871. [Wa, Wm, 

1908. — Dysenteric amoebae and liver abscess. [Read before 76. Ann. Meet. 

Brit. Med. Ass., Sheffield, July] <Brit. M. J., Lond. (2495), v. 2, Oct. 24, 

pp. 1252-1253. [Wa, Wm.] 
1909. — Amibes dysenteriques et suppuration du foie <Presse med., Par., 

v. 17 (4), 13 Jan., p. 27. [Wa, Wm.] 

Marshall. D. G. [Major, Indian Med. Serv. ; Lecturer, Trop. Dis., School Med., 

Roy. College, Edinburgh.] 
1899 a. — The Amoeba dysenteriae: Its relation to tropical abscess of the 

liver <Brit. M. J., Lond. (2006), v. 1, June 10, pp. 1386-1388, figs. 1-5. 

[Wa, Wm.] 
(1912). — A case of amoebic dysentery occurring in a man who had never 

been out of Scotland <Edinb. M. J., Mar. 
1912.— Idem <J. Trop. M. & Hyg., Lond., v. 15 (7), Apr. 1, pp. 108-110. 

[Wa, Wm.] 

Marshall, Harry T. [Dr.] 

1909. — An unusual case of amoebic dysentery. [Read before Am. Ass. Path. 

& Bacteriol., Apr. 9] <Philippine J. Sc, Manila, v. 4 (5), Oct., pp. 303- 

307, 1 pi. [Wa.] 
Martin, Charles F. [M. D.] 

1911. — Dysentery <Handb. Pract. Treat. (Musser & Kelly), Phila. & Lond., 

v. 2, pp. 643-657. [Wm.] 
Martin, C. H. [M. A.] 

1911. — Contributions to the study of pathogenic amoebae from Bombay. 

Part 2. Descriptions of preparations of amoebae from Major Liston's 

cultures < Quart. J. Micr. Sc, Lond., n. s. (226), v. 57 (2), Nov., pp. 122- 

128, pis. 16-18, figs. 1-32. [MS. dated Apr. 4.] [Wa, Wm.] [For pt. 1, 

see Liston, W. Glen, 1911, pp. 107-122; 127-128.] 
1911. — A note on the early stages of nuclear divisions of the large amoeba 

from liver-abscesses < Ibidem, pp. 279-281, figs. 1-7. [Wa, Wm.] 

Martin, F. S. [M. D., Beaumont, Texas.] 

1905 a.— Dysentery <Charlotte [N. C] M. J., v. 26 (6), June, pp. 378-381. 

Martini. [Prof. Dr.] 

1908. — Amobentrager <Arch. f. Schiffs- u. Tropen-Hyg., Leipz., v. 12 (18), 

Sept., pp. 588-591. [MS. dated 2. Juni.] [Wm.] 
1910. — Ueber einen bei amobenruhrahnlichen Dysenterien vorkommenden 

Ciliaten <Ztschr. f. Hyg. u. Infektionskrankh., Leipz., v. 67 (3), 31. Dec., 

pp. 387-390, 1 fig. [Wa, Wm.] 


Ma rtini — Continued. 

1911. — Mikrobiologischo Hrfahruugen bei den epidemischen Bemerkungen 
des Schutzgebietes Kiautschou und der Provinz Schantung in den Jahren 
1907 bis 1911 <Ztsehr. f. Hyg. u. Infektionskrankh., Leipz., v. 69 (2), 12. 
Sept., pp. 37G-39G. [Wa, Win.] 
Marvel, Philip. [Dr., Atlantic City, N. J.] 

1903 a. — A case of Amoeba coli dysentery. [Secretary's abstract of paper 
read before 137. Ann. Meet. Med. Soc. New Jersey, June 23] <Med. Rec., 
N. Y. (170S), v. 64 (5), Aug. 1, p. 194. [Wa, Wm.] 
Masyutin, N. G. 

1889 a. — Demonstration bolnai, stradayushai Amoeba coli. [Demonstra- 
tion of a patient with Amoeba coli.] [Russian text] <Protok. zasaid. 
Obsh. Kievsk. vrach (1888-89), pp. 60-64. [Wm.] 
1889 b. — Ob amebakh, kak chuzheyadnfkh tolstikh hishek. [Amoebae as 
parasites of the large intestines.] [Russian text] <Vrach, St. Petersb., 
v. 10 (25), 22 yunia, pp. 557-559. [Wm.] 
Mathis, C. ; & Leger, M. 

1911. — Recherches de parasitologic et de pathologie humaine et animales au 
Tonkin, viii+1 p. 1.+451 pp., 24 figs., 14 pis. 8°. Paris. [Wa.] 
Mathis, C. ; Leger, M. ; & Jouvenu-Dubreuil. 

(1911). — Diminution du taux des eosinophils dans l'hepatite suppuree ami- 

bienne <Rull. Soc. m€d. chir. de l'lndo-Chine, v. 2, pp. 28-42. 
(1911). — Du taux des eosinophils dans la dysenterie amibienne <Ibldem 

p. 200. 
1912.— Idem. [Abstract by M. Leger] <Bull. de l'Inst. Pasteur, Par., v. 10 

(9), 15 mai, p. 405. [Wa, Wm.] 
1912. — Diminution du taux des eosinophils dans l'hepatite suppuree ami- 
bienne. [Abstract of 1911, pp. 28-42, by M. Leger] < Ibidem, pp. 405-406. 
[Wa, Wm.] 
Matthews, E. A. C. [M. A., M. B. Cantab.; Capt. I. M. S. ; 10th D. C. O. 
1905. — The etiology of dysentery with some notes on treatment < Indian M. 
Gaz., Calcutta, v. 40 (7), July, pp. 253-257, figs. 1-3. [Wm.] 
Maxwell, James L. [Dr., Formosa.] 

1908. — [Tropical abscess of liver.] [Abstract of discussion before 76. Ann, 
Meet. Brit. Med. Ass., Sheffield, July] <Brit. M. J., Lond. (2495), v. 2, 
Oct. 24, p. 1254. [Wa, Wm.] 
Maxwell, J. Preston. [M. B., F. R. C. S., Yung-Chun, Amoy.] 

(1909). — Rare cases from the Fukien Province. South China. A case of 
amoebic abscess of the spleen <Tr. Soc. Trop. M. & Hyg., Lond., v. 2 (9). 
1909.— Idem. [Abstract] <Trop. M. & Hyg., Lond., v. 12 (16), Aug. 16, 
p. 248; discussion, pp. 248-249. [Wa, Wm.] 
Mayer, August Franz Joseph Karl. [Dr., Prof., Anat. u. Physiol, a. d. k. preuss. 
Rhein. Univ., Bonn*] 
1843 a. — Spicilegium observationum anatomicarum de organo electrico in 
Raiis anelectricis et de haeinatozois. 17 pp., 3 pis. 4°. Ronnae. [Wa.] 
Meisenbach, A. H. [Dr.] 

1902.— [Discussion of Nietert, H. L., 1902, pp. 55-61] <St. Louis Med. Rev. 
(1901), v. 46 (4), July 23, p. 65. [Wm.] 
Menetrier, P. [Dr. ; Prof. agreg6 a la Fac. de med. ; M6d. de 1'hCp., Tenon.] 

1910. — Sur un cas de salpingite amibienne. [Abstract of remarks before 
Acad, de m§d., 31 mai, by Ph. Pagniez] <Presse med., Par., v. 18 (44), 
l er juin, p. 415. [Wa, Wm.] 

66692— vol 2, pt 1—13 16 


Menetrier, P. — Continued. 

1910. — Salpingite amibienne <Arch. de parasitol., Par., v. 14 (1), 30 juillet, 
pp. 154-159, figs. 1-2. [Wa, Wm.] 
Menetrier, P.; & Touraine, A. [Interne d. h6p.]. 

1908. — AbscSs amibienne du foie. Phag£deuisme cutanS amibien. [Read 12 
juin] <Bull. et niem. Soc. m6d. d. h6p. de Par., 3. s., v. 25, pp. 905-913, 
1 fig. ; discussion, pp. 913-914. [Wm.] 

Mercier, L. [Chef d. trav. de zool., Fac. d. sc, Nancy.] 

1907. — Un parasite du noyau d'Amoeba blattae Biitschli [Read 10 juin] 

<Compt. rend. Soc. de biol., Par., an. 59, v. 62, v. 1 (21), 21 juin, pp. 

1132-1134. [Wa, Wm.] 
1908. — La schizogonie simple chez Amoeba blattae Biitschli <Compt. rend. 

Acad. d. sc, Par., v. 146 (18), 4 mai, pp. 942-945. [Wa, Wm, Wc] 
1909. — Le cycle evolutif d' Amoeba blattae Biitschli. (Note preliminaire) 

<Arch. f. Protistenk., Jena, v. 16 (2), pp. 164-168. [MS. dated Mar. 10.] 

[Wa, Wm.] 
1910. — Contribution a l'Stude de l'amibe de la blatte (Entamoeba blattae 

Biitschli) <Ibidem, v. 20 (2), pp. 143-175, figs. I-VI, pis. 10-12, figs. 1-63 


von Mereschkowsky, C. [St. Petersburg.] 

1878 a. — Studien fiber Protozoen des nordlichen Russland <Arch. f. mikr. 
Anat, Bonn, v. 16 (2), 20. Dec., pp. 153-248, pis. 10-11. [Wm.] 
Messineo, Giuseppe. [Dr., Capitano med., Asst. onorario.] 

1911. — Contribute alio studio delle enterocolite da amebe <Gazz. med. ital., 
Torino, v. 62 (25), 22 giugno, pp. 241-244. [Wm.] 

Metcalf, Maynard M. [Prof., Zool., Oberlin College.] 

1910. — Studies upon amoeba <J. Exper. Zool., Phila., v. 9 (2), Oct., pp. 
301-331, figs. 1-45. [Wa.] 

Mgtin, B. ; & Guillon, A. 

1908. — Dysenterie et vers intestinaux a propos d'un cas de dysenterie tropi- 
cale a 6tiologie complexe <Rev. de m6d. et d'hyg. trop., Par., v. 5 (2), 
pp. 98-102. [Wm.] 

Meyer, H. [Dr., Dresden.] 

1906. — Ueber chronische Dysenterie und ihre Behandlung. [Read before 
Freien Ver. f. inn. Med. Konigr. Sachsen, 24. Mai] <Deutsche med. 
Wchnschr., Leipz., v. 32 (33), 16. Aug., pp. 1327-1330. [Wa, Wm.] 

Milks, H. J. [D. V. M., Asst. Vet. & Bacteriol.] 

1908. — A preliminary report on some diseases of chickens <Bull. 108, 
Louisiana Agric. Exper. Station, Baton Rouge, Aug., 11 pp., 4 pis., figs. 
1-4. [Wa.] 

Miller, Casper O. [Dr. med.] 

1894 a. — Ueber aseptische Protozoenkulturen und die dazu verwendeten 

Methoden <Centralbl. f. Bakteriol. [etc.], Jena, v. 16 (7), 25. Aug., pp. 

273-280. [Wa, Wm, Wc] 
Minchln, Edward Alfred. [M. A.; Prof., Zool., Univ. College, London.] 

1907.— Protozoa <Syst Med. (Allbutt & Rolleston), Lond., v. 2 (2), pp. 

9-122, figs. 1-82. [Wm.] 
1909.— Protozoa < Ibidem, pp. 9-122, figs. 1-82. [Wa.] 
1910. — On some parasites observed in the rat-flea (Ceratophyllus fasciatus) 

<Festschr. z. 60. Geburtst. Richard Hertwigs (Mtinchen), Jena, v. 1, pp. 

289-302, pi. 23, figs. 1-11. [MS. dated Feb. 22.] [Wm.] 


Miura, Kinnosuke. [Dr.; Prof., Univ. Tokyo.] 

1900. — Amobenbefund in der Punctionsflilssigkeit bei Tumoren der Peri- 
toneal liohle. 18 pp.. 4 figs. 4°. Tokio. [Lib. Stiles.] 
1901.— Idem <Mitth. a. d. med. Fac. d. k.-.1ap. Univ. zu Tokio, v. 5 (1), 
pp. 1-18, figs. 1-4. [Wm.] 
Molisch, Hans. 

1903 a. — Amoeben als parasiten in Volvox <Ber. d. deutsch. bot. Ge- 
sellsch., Bed., v. 21 (1), 25. Feb., pp. 20-23, pi. 3, figs. 1-5. [Wa.] 
Moniez, R[omain-Louis]. 

1896 a. — Trait6 de parasitologic animale et veggtale appliquee a la medi- 
cine. viii+680 pp., 116 figs. 8°. Paris. [Wa, Wm.] 
Morgenroth. [Dr., Stabsarzt.] 

1904. — Ueber Ruhruntersuchungen in China, in besonderen fiber die Bak- 
terienarten, die bei chinesiscber Ruhr gefunden und durch Blutserum ag- 
glutiniert wurden <Arch. f. Schiffs- n. Tropen-Hyg., Leipz., v. 8 (1), pp. 
27-35. [Wm.] 
Moroff, Theodor. [Dr., k. bayer. biol. Versuchsstation f. Fischerei, Mtinchen.] 
1908. — Die bei den Cephalopoden vorkommenden Aggregataarten als Grund- 
lage einer kritischen Studie fiber die Physiologie des Zellkernes <Arch. 
f. Protistenk., Jena, v. 11 (1), pp. 1-224, 74 figs., pis. 1-11, figs. 1-103 e, 
[Wa, Wm.] 
Mosler, [Karl] Friedrich [Dr.. Docent u- klin Asst.-Arzt, Giessen] ; & Peiper, 
1894 a. — Thierische Parasiten <Spec. Path. u. Therap., . . . Nothnagel, 
Wien, v. 6, xii+345 pp., 124 figs. [Wm.] 
Motas, C. S. [Prof., Ecole supe'r. de m6d. v€t, de Bucarest.] 

1906. — Le role des protozoaires dans les maladies des animaux <Rep. 8. 
Internat. Vet. Cong., Budapest, 1905, v. 2, pp. 681-698. [Wa.] 
Moulden, William R. [Dr., Washington, D. C] 

1906 a. — Comparative treatment of intestinal amebiasis <Med. Rec, N. Y. 

(1864), v. 70 (4), July 28, pp. 132-135. [Wa, Wm.] 
1908. — Tratamiento de la disenteria amibiana por las inyecciones rectalee 
de sulfato de cobre. [Editorial abstract] <Habana med., v. 11 (10), 
oct., p. 78. [Wa, Wm.] 
Miiller, Oskar. [M. D., Hongkong.] 

1912. — The surgical treatment of dysentery. [Secretary's abstract of paper 
read before 2. bien. Cong. Far East. Ass. Trop. M., Hong Kong] <J. 
Trop. M. & Hyg., Lond., v. 15 (20), Oct. 15, pp. 314-315. [Wa, Wm.] 
Mugliston, T. C. ; & Freer, G. D. [Colonial Surgeons, Penang.] 

1905 a. — An undescribed form of ulceration of the large intestine, probably 
of amoebic origin, causing in some cases abscess of the liver <J. Trop. 
M., Lond., v. 8 (8), Apr. 15, pp. 113-115, 2 figs. [Wa. Wm.] 
Munro, John C. ; & Councilman, William T. [M. D.'s.] 

1897. — A case of amoebic abscesses of the liver, with autopsy <Med. & Surg. 
Rep. Bost. City Hosp., 8. s., pp 352-358. [Wm.] 

Murphy, Franklin E. [M. D., Kansas City, Mo.] 

1894.— A case of amoebic dysentery <J. Am M. Ass.. Chicago, v. 22 (5), 
Feb. 3, p. 149. [Wm.] 

Murray, Francis W. [M. D., New York.] 

1901. — The surgical treatment of amoebic dysentery. [Read at Meet. Hosp. 
Graduates' Club, Oct. 25, 1900] <Ann Surg., Phila., v. 33 (5) [May], 
pp. 574-581. [Wm.] 


Musgrave, William E. [M. D. ; Path., Govt. Lab. ; Physician, St. Paul's Hosp., 
Manila, P. I.] 

1904 a. — Treatment of intestinal amebiasis (amebic dysentery) in the 
tropics < [Publication] (18), Bureau Govt. Lab., Manila, Oct., pp. 87-117. 

1905 d.— Idem <J. Am. M. Ass., Chicago, v. 44 (14), Apr. 8, pp. 1098-1107. 
[Wa, Wm, Wa] 

1905 1. — Symptoms, diagnosis and prognosis of uncomplicated intestinal 
amebiasis in the tropics. [Read before 56. Ann. Sess. Am. Med. Ass., 
July 11-14] <J. Am. M. Ass., Chicago, v. 45 (12), Sept. 16, pp. 830-837. 
[Wa, Wm, Wa] 

1906 a. — Amoebiasis : Its association with other diseases, its complications, 
and its after effects. [Abstract of paper read before Philippine Islands 
Med. Ass., Mar. 3] <Philippine J. Sc, Manila, v. 1 (5), June, pp. 547-573. 
[Wa, Wm.] 

1910. — Intestinal amoebiasis without diarrhoea. A study of fifty fatal 
cases <Ibidem, v. 5 (2), July, pp. 229-231. [Wa, Wm.] 

1912. — The treatment of intestinal amebiasis. [Read before 62. Ann. Sess., 
Los Angeles, June, 1911] <J. Am. M. Ass., Chicago, v. 58 (1), Jan. 6, 
pp. 13-17 ; discussion, pp. 17-18. [Wa, Wm, Wa] 

Musgrave, William E. ; & Clegg, Moses T. [Asst. Bacteriol., Biol. Lab.]. 

1903 a. — Trypanosoma and trypanosomiasis, with special reference to surra 
in the Philippine Islands < [Publication] (5), Bureau Govt. Lab., Manila, 
248 pp., figs. 1-155. [Wa.] 

1904 h. — Amebas: Their cultivation and etiologic significance < [Publica- 
tion] (18), Bureau Govt. Lab., Manila, Oct., pp. 5-85, pis., figs. 1-3, 1-32. 

1905 m. — Amebas : Their cultivation and etiological significance < J. Infect. 
Dis., Chicago, v. 2 (2), Mar. 1, pp. 334-350, pi. 12, figs. 1-4. [Wa, Wm.] 

1906. — The cultivation and pathogenesis of amoebae <Philippine J. Sc, 

Manila, v. 1 (9), Nov., pp. 909-950, 5 pis., figs. 1-10. [Wa, Wm.] 
Musser, John H. [Asst. Prof., Clin. Med., Univ. Penn.] 

1890 a. — Some clinical remarks on dysentery <Univ. M. Mag., Phila., v. 3 

(3), Dec, pp. 116-124. [Wm.] 
1900 b. — [Note on tropical dysentery.] [Abstract of paper read before 51. 

Ann. Meet. Am. Med. Ass., Atlantic City, June 5] <Phila. M. J. (128), 

v. 5 (23), June 9, pp. 1262-1263. [Wa, Wm.] 
1902 a.— [Discussion on dysentery] <Brit. M. J.. Lond. (2177), v. 2, Sept 

20, p. 851. [Wa, Wm.] 

Musser, John H. ; & Willard, De Forest. 

1893 a. — A case of abscess of the liver following amebic dysentery, with 

remarks <Univ. M. Mag., Phila., v. 5 (7), Apr., pp. 525-530. [Wm.] 
1893. — A case of abscess of the iiver following amoebic dysentery: With 

remarks. [Read Feb. 22] <Proc. Phila. Co. M. Soc., Phila., v. 14, 

pp. 100-105; discussion, p. 105. [Wm.] 
1904. — Infection in the upper abdomen: Probably an abscess of the liver of 

amebic origin. [Read Mar. 23] <Ibidem, v. 25. n. s., v. 6 (4), Apr. 30, 

pp. 115-118. [Wm.] 
Myer, Jesse S. [M. D., St. Louis, Mo.] 

1002 a.— Endemic amebic dysentery. [Read before St. Louis Med. Soc., 

Apr. 19] <St. Louis Med. Rev. (1089), v. 46 (2), July 12, pp. 19-26, 

figs. 1-4. [Wm.] 


Njiogler, Kurt. [Dr.] 

1909. — Entwioklungsgeschichtliche Studien fiber Auioben <Arch. f. Protis- 

tenk., Jena, v. 15 (1-2), pp. 1-53, pis. 1-6, figs. 1-139. [Wa, Win.] 
1910. — Fakultath parasitische Mierococcen in Amoben <Ibidem, v. 19 (3), 

pp. 240-254. pj. 10, figs. 1-24. [Wa, Win.] 
1911. — Studies iiber Protozoen aus einem Alintiiinpel. 1. Amoeba hartmanni 
n. sp. An hang: Zur Centriolfrage <Ibidem, v. 22 (1). pp. 56-70, pi. 7, 
figs. 1-32. [Wa, Win.] 
Nasse, D. [Asst. Arzt, k. cbir. Univ. -Klin.] 

1891 a. — Ueber einen Aniobenbefund bei Leberabscessen, Dysenterie und 
Nosocomialgangran <Arb. a. d. cbir. Klin. d. k. Univ. Berk, v. 5, pp. 
95-109. [Win.] 
1892a.— Idem <Arcb. f. klin. Cbir., Berl., v. 43 (1), pp. 40-54. [Wm.] 
Nat tan-La rrier, L. [Dr.; Chef de clin., Fac. de med. a l'Hotel-Dieu.] 

1907. — Un nouveau cas d'abces dysenterique du pouinon <Rev. de med. et 
d'byg. trop., Par., v. 4 (2), pp. 60-62; discussion, pp. 62-63. [Wm.] 
Neresheiruer, Eugen. 

1908. — Zur Fortpflanzung eines parasitiscben Infusors (Ichtbyopbthirius). 
[Read before Gesellscb. f. Morpbol. u. Physiol, in Miinchen, 3. Dec] 
<Miinchen. med. Wchnscbr., v. 55 (1), 7. Jan., pp. 48-50. [Wa, Wm.] 
Neveu-Lemaire, Maurice. [Dr. ; Prof, agrege a la Fac. de med. de Lyon.] 

1902 a. — Parasitologie animale. A l'usage des candidats au 3 e examen de 
doctorat (2 e partie). Et une preface par R. Blanchard. iii+212 pp., 
301 figs. 12°. Paris. [Wa, Wm.] 
1904 a.— Parasitologie animale. Et une preface par R. Blanchard. 2. ed., 

iii+220 pp., 301 figs. 12°. Paris. [Wa, Wm.] 
1912. — Parasitologie des animaux domestiques. Maladies parasitaires non 
bacteriennes. ii+1257 pp., 770 figs. 12°. Paris. [Wa, Wm.] 
Newell, A. G. [M. D., D. P. H., Calcutta.] 

1905. — Dysentery : Its varieties and causes, summarised and criticised, with 
a note on treatment and prevention <Indian M. Gaz., Calcutta, v. 40 (7), 
July, pp. 257-260. [Wm.] 
Newell, H. A. [M. D.. Louisburg, N. C] 

1910. — A study of some parasitic diseases. [Read before N. Carolina Med. 

Soc, June] <Charlotte [N. C] M. J., v. 62 (2), Aug., pp. 97-100. [Wm.] 

Nichols, Henry J. [Capt, Med. Corps, U. S. Army] ; & Phalen, J. M. [Capt, 

Med. Corps, U. S. Army]. 

190S. — The work of the board for the study of tropical diseases in the 

Philippines <Mil. Surg., Carlisle, Pa., v. 23 (5), Nov., pp. 361-370. [Wm.] 

Nietert, H. L. [M. D., St. Louis; Supt, City Hosp.] 

1902. — Dysentery — report of nine cases. [Read before St. Louis Med. Soc, 
Apr. 19] <St. Louis Med. Rev. (1091), v. 46 (4), July 26, pp. 55-61; 
discussion, p. 65. [Wm.] 
Niles, George M. [M. D., Atlanta, Ga.] 

1908. — Some remarks on amoebic dysentery. [Read before Fulton Co. Med. 
Soc] <Atlanta Jour.-Rec Med., v. 10 (8), Nov., pp. 420-424. [Wm.] 
Noc, F. [Dr., Med. major d. troupes colon.] 

1909. — Recherches sur la dysenterie amibienne en Cochinchine <Aun. de 
l'Inst. Pasteur, Par., v. 23 (3), 25 mars, pp. 177-204, pis. 10-13. [Wa, 
Noeller, Wilhelm. [Stud. med. vet.] 

1912. — Entamoeba aulastomi nov. spec, eine neue parasitische Amobe aus 
dem Pferdeegel (Aulastomum gulo Moq.-Tand.) <Arch. f. Protistenk., 
Jena, v 24 (3). pp. 195-200, pi. 19, figs. 1-22. [Wa, Wm] 


Norcnand, A. [Dr., ined. princip., division de Chine et du Japon.] 

1879 a. — Note sur deux cas de colite parasitaire <Arch. de m£d. nav., Par., 
v. 32 (9), sept, pp. 211-218, figs. 1-7. [Wm.] 
Nothnagel, Carl Wilhelm Hermann. 

1884 a. — Beitrage zur Physiologie und Pathologie des Darmes. 3 p. L, 249 
pp., 2 pis. 8°. Berlin. [Wm.] 

Nydegger, James A. [M. D., Surg., U. S. Pub. Health & Mar.-Hosp. Serv., 
Pittsburg, Pa.] 

1907. — Amebic dysentery in sailors at the port of New York <West Vir- 
ginia M. J., Wheeling, v. 2 (1), July, pp. 11-15. [Wm.] 

1910. — Some remarks on the extent of prevalence, the etiology and treat- 
ment of amebic dysentery <Penn. M. J., Athens, v. 13 (8), May, pp. 
633-638. [Wm.] 

1910. — Amebic dysentery; its prevalence, etiology and treatment <West 
Virginia M. J., Wheeling (1909-10), v. 4 (12), June, pp. 399-105. [Wm.] 
Ogata, Masanori. [Prof., Hyg. Inst., Univ. zu Tokio.] 

(1893 a). — Kenshu no sunjotsu baiyo ni zukete. [Pure cultures of Infu- 
soria.] [Japanese text] <Chiugai Iji Shinpo, Tokio (318), pp. 1-6. 

1893 b. — Ueber die Reinkultur gewisser Protozoen (Infusorien). [Transl. 
of 1893 a] <Centralbl. f. Bakteriol. [etc.], Jena, v. 14 (6), 7. Aug., pp. 
165-169. [MS. dated 19. Mai.] [Wa, Wm, Wc] 

de Oliveira, Olinto. [Dr., Prof., clin. pedriatica, faculdade de med., Porto 

1904 b. — A dysenteria amebica na infancia. [Read before 2. Cong. Med.- 

Latin-Amer., Buenos Aires, abril] <Brazil-med., Rio de Jan., v. 18 (32), 

22 agosto, pp. 321-323; (33), 1 settembre, pp. 331-334; (34), 8 settembre, 

pp. 341-345. [Wm.] 
1905. — 'La dysenterie amibienne chez l'enfant <Arch. de med. d. enf., Par., 

v. 8 (4), avril, pp. 193-213. [Wm.] 

Olney, T. A. [Dr., Chicago, 111.] 

1896. — A report of a case of amoebic liver abscess. [Abstract of paper 
read May 13, 1895] <Tr. Chicago Path. Soc. (Oct, 1894-Nov., 1895), 
v. 1, pp. 199-200; discussion, pp. 200-201. [Wm.] 

Opie, Eugene Lindsay. [Dr.; Ass., Path., Johns Hopkins Univ.; Fellow, Rocke- 
feller Inst. Med. Research.] 
1901. — Healed amoebic abscess of the liver, and amoebic abscess of the 
lung. Exhibitions of specimens < Johns Hopkins Hosp. Bull., Bait. (124), 
v. 32, July, p. 219. [Wa, Wm.] 
Oppenheim, Nathan. [Attend. Pays., Child. Dept, Mt. Sinai Hosp. Dispen., 
New York.] 
1900 a. — The medical diseases of childhood, xx pp., 1 p. l.-f-653 pp., 121 
figs., frontispiece. 8°. New York. [Wm.] 

Osborn, Samuel. [Dr.] 

1904 a. — Amebic dysentery, Trichomonas intestinalis, Anchylostomum duo- 
denale and Trichoccphalus dispar in the same patient. [Abstract of 
paper read before Clin. Soc. Hosp., Univ. Michigan, Mar. 30] <Physi- 
cian & Surg., Detroit & Ann Arbor (304), v. 26 (4), Apr., pp. 164-167. 

Osier, (Sir) William. [M. D., Regius Prof., Med., Oxford Univ., England.] 
1890 b. — On the Amoeba coli in dysentery and in dysenteric liver abscess 
< Johns Hopkins Hosp. Bull., Bait., v. 1 (5), May, pp. 53-54. [Wm, Wc] 


Osier, (Sir) William— Continued. 

1890 d. — Ueber die in Dysenterie und dysenterischem Leberabscess vor- 

handene Amoeba <Centralbl. f. Bakteriol. [etc.], Jena, v. 7 (23), 31. 

Mai, pp. 736-737. [MS. dated 10. Apr.] [Wa, Wm, Wc] 
1895. — Abscess of the liver, perforating the lung. [Remarks before Johns 

Hopkins Hosp. Med. Soc, Oct. 7] < Johns Hopkins Hosp. Bull., Bait. 

(54-55), v. 6, Sept.-Oct, p. 144. [Wa, Wm.] 
1898 a. — The principles and practice of medicine; designed for the use of 

practitioners and students of medicine 3. ed., xvi pp., 1 p. 1., 1181 pp. 

8°. New York. [Wm, Wc] 
1902 c. — On amebic abscess of the liver. [Clinical lecture delivered at 

Johns Hopkins Hosp., Feb. 15] <Med. News, N. Y. (1526), v. 80 (15), 

Apr. 12, pp. 673-677, charts 1-3. [Wa, Wm, Wc] 
1902 g. — Amebic dysentery. [Remarks before Phila. County Med. Soc, 

Mar. 26] <Therap. Gaz., Detroit, v. 26, 3. s., v. 18 (4), Apr. 15, pp. 217- 

218. [Wa, Wm.] 
Paquin, Paul. [Dr., Asheville, N. C] 

1905.— [Discussion of Tuttle, James P., 1905, pp. 348-353] <Lancet- 

Clinic, Cincin., v. 94, n. s., v. 55, Sept. 23, pp. 354-355. [Wm.] 
Pasquale, Allessandro. 

1893 a. — Spedizione scientifica Kruse-Pasquale per lo studio della dissen- 
teria e dell'ascesso epatico in Egitto <Gior. med. d. r. esercito [etc.], 
Roma, v. 41 (2), feb., pp. 176-189. [Wm.] 

Patterson, Henry S. [M. D. ; Assoc, Applied Therap., College Phys. & Surg., 

Columbia Univ., New York.] 
1908. — Parasites found in New York City <Arch. Int. Med., Chicago, v. 2 

(2), Sept. 15, pp. 185-193. [Wm.] 
1909. — Endemic amoebic dysentery in New York, with a review of its dis- 
tribution in North America <Am. J. M. Sc, Phila. & N. Y., n. s. (449), 

v. 138 (2), Aug., pp. 19&-202. [Wm.] 
1910. — Amebic dysentery in New York. [Read before N. York Acad. Med., 

Nov. 6, 1909] <Med. Rec, N. Y. (2062), v. 77 (20), May 14, pp. 835- 

836. [Wa, Wm.] 
Pearce, Richard M. [Prof., Univ. Penn.] 

1912. — Research in medicine. [Hitchcock lectures, delivered at Univ. 

Calif., Jan. 23-26] <Pop. Sc Month., N. Y., v. 81 (2), Aug., pp. 115-132. 

Peck, A. E. [Surg., U. S. Navy.] 

1910. — Report of a case of amoebiasis <U. S. Naval Med. Bull., Wash., v. 

4 (1), Jan., pp. 51-54. [W,a, Wm.] 
Penard, Eugene. [Dr. Sc] 

1904 a. — Quelques nouveaux rhizopodes d'ean douce <Arch. f. Protistenk., 

Jena, v. 3 (3), pp. 391-422, 11 figs. [Wa, Wm.] 
1909. — Sur quelques rhizopodes des mousses < Ibidem, v. 17 (2), pp. 258- 

296, 36 figs. [Wa, Wm.] 
Perroncito, Edoardo. [Prof., r. Univ. Torino.] 

1882 a. — I parassiti dell'uomo e degli animali utili. Delle piu comuni 

malattie da essi prodotte. profilassi e cura relativa. xii+506 pp., 233 

figs., 14 pis. 8°. Milano. [Wa, Wm.] 

1894 b. — [Ameba intestinale.] [Secretary's abstract of remarks, 16 mar.] 
<Gior. r. Accad. di med. di Torino, an. 57 [3. s.]. v. 42 (3), mar., p. 177. 
[Wm, Wc] 


Perroncito, Edoardo — Continued. 

1894. — Di un' ameba intestinale. [Remarks before Accad. med. di Torino, 
13 mar.] <Riforina raed., Napoli, an. 10, v. 1 (72), 28 mar., p. 859. 
1912. — [L'enkystement des germes morbides et les maladies dont ils sont la 
cause specifique.] [Remarks before 19. Gen. Ann. Assembly, 27 few] 
<Bull. Soc. zool. de France, Par., v. 37 (2), 5 avril, pp. 26-38. [Wa.j 
Perroncito, Edoardo; & Bosso, G. 

1896. — Sullo sviluppo e proliferazione d.elYAme'ba. [Read 10 gennaio] 
<Gior. r. Acad, di med. di Torino, an. 59, 4. s., v. 2 (2), feb., pp. 91-93. 
Petersen, Edward W. f Adjunct Prof., Surg., N. York Post-Graduate Med. 
1905 a. — A case of amebic dysentery treated by appendicostomy <Post- 
Graduate, N. Y.. v. 20 (7), July, pp. 714-717. [Wm.] 
Petrone, Luigi M. 

1884 a. — Nota sulP infezione dissenterica <Sperimentale, Pirenze, an. 38 
[4. s.], v. 53 (5), maggio, pp. 509-515. [Wm.J 
Peyrot [Dr.] ; & Roger [Prof, agrege & la Fac. de med. de Paris]. 

1896 a. — Abces dysenteriques du foie avec amibes <Gaz. d. h6p., Par., v. 69 

(42), 7 & 9 avril, p. 435. [Wm.] 
1896 b.— Idem <Med. mod., Par., v. 7 (29), 8 avril, p. 232. [Wm.] 
1896. — Abces dysenterique du foie ne contenant que des amibes. [Read 
before Acad, de med., 7 avril] <Semaine med., Par., v. 16 (18), 8 avril, 
p. 143. [Wm.] 
1897. — Sur un cas d'abces dysenterique du foie ne contenant que des amibes 
<Rev. de chir., Par., v. 17 (2), 10 few, pp. 89-99, figs. A-E. [Wm.] 
Pfeiffer, Ludwig (sr.). [Dr., Weimar.] 

1888 c. — Weitere TJntersuchungeu iiber Parasiten im Blut und in der Lymphe 
bei den Packenprocessen <Cor.-Bl. d. allg. arztl. Ver. v. Thuringen, 
Weimar, v. 17 (11), 25. Nov., pp. 644-667, pis. 1-10. [Wm.] 

1890 c. — Unsere heutige Kenntniss von den pathogenen Protozoen <Cen- 
tralbl. f. Bakteriol. [etc.]. Jena, v. 8 (24), 4. Dec, pp. 761-768; (25), 11. 
Dec, pp. 794-803. [MS. dated 8. Nov.] [Wa, Wm, Wc] 

1891 a. — Die Protozoen als Krankheitserreger, sowie der Zellen und Zellen- 
kernparasitismus derselben bei nicht-bakteriellen Infektionskrankbeiten 
des Menscben. 2. sebr vermehrte Aufl. vi+216 pp., 91 figs. 8°. Jena, 
[Wa, Wm.] 

Pfeiffer, R. [Prof. Dr.] 

1892 a. — Beitrage zur Protozoen-Forschning. 1. Heft: Die Coccidien- 
Krankheit der Kaninchen. 24 pp., 12 pis. 8°. Berlin. [Wm.] 

Phalen, James M. ; & Nichols. Henry J. 

1908. — Tropical diseases in the Philippines <Mil. Surg., Carlisle, Pa., v. 23 
(6), Dec, pp. 462-468. [Wm.] 
Phoustanos, Joannis A. 

1906. — [Amoebic dysentery, or enteric amoebism; on amoebic typhlocolitis.] 
[Greek text] < f IarpiKT} npddos, 'Eu Xvpw, v. 11, pp. 65-69, figs. 1-2; pp. 
97-104, figs. 3-6. [Wm.] 

Piccardi, Girolamo. [Dr., 1st. Parassit., Univ. di Torino.] 

1895 a. — Alcuni protozoi delle feci dell'uomo. [Read 14 die 1894] <Gior. r. 
Accad. di med. di Torino, an. 58, 4. s., v. 1 (3-4), mar.-apr., pp. 169-186, 
1 pi., figs. 1-9. [Wm.l 


Plehn, Albert. [Dr., Regierungsarzt, Kamerun.] 

1898 a. — Die Dysenterie in Kamerun <Arch. f. Schiffs- u. Tropen-Hyg., 
Leipz., v. 2 (3), Juni, pp. 125-133. [Wm.] 

Popoff, Methodi. [Dr., Dozent d. Zool., Univ. Sofia, Bulgaria.] 

1911. — Ueber den Entwieklungscyclus von Amoeba minuta n. sp. Anhang: 
Ueber die Teilung von Amoeba sp. <Arch. f. Protistenk., Jena, v. 22 
(2), pp. 197-223, figs. 1-7, pis. 13-14, figs. 1-31. [Wa, Wm.] 
Porter, Annie. [B. Sc. Lond. ; Zool. Kes. Lab., Univ. College, London.] 

1909. — Amoeba chironomi, nov. sp., parasitic in the alimentary tract of the 
larva of a Chironomus <Parasitology, Cambridge [Eng.], v. 2 (1-2), 
May-June, pp. 32-41, figs. 1-21. [Published July 13.] IWa.] 
Posner, C. 

1893 a. — [Amoeben.] [Secretary's abstract of remarks before Ver. f. inn. 
Med., 18. Juli] <Deutsche med. Wchnschr., Leipz. & Berl., v. 19 (7), 16. 
Feb., p. 166. [Wa, Wm.] 

1893 c. — Ueber Amoeben im Harne. Vortrag gehalten in der Hufeland- 
'schen Gesellschaft zu Berlin <Berl. klin. Wchnschr., v. 30 (28), 10. 
Juli, pp. 674-676, figs. a-d. [Wa, Wm.] 


1911. — Abc§s amibienne du cerveau, mStastase d'abces de meme nature du 
foie et du poumon ; mort [Abstract of paper read before Soc. de chir., 
l er fev., by J. Dumont] <Presse med., Par., v. 19 (10), 4 fev., p. 94. 
[Wa, Wm.] 

Potieenko, V. V. 

1899. — Mnozhestvennyi gnoinik pecheni na pochvie amebnago zarazhenila. 
[Multiple abscess of the liver resulting from amoebic infection.] [Rus- 
sian text] <Med. Obozr., Mosk., God 26, v. 51 (3), mart, pp. 530-539. 

Powell, A. [Capt. I. M. S. retired, Bombay.] 

1908. — Tropical abscess of liver.] [Abstract of discussion before 76. Ann. 
Meet. Brit. Med. Ass., Sheffield, July] < Brit. M. J., Lond. (2495), v. 2, 
Oct. 24, p. 1254. [Wa, Wm.] 

Preble, Robert B. [M. D. ; Prof., Med., Northwest. Univ. Med. School, Chicago, 

1899 a. — Amebic dysentery in Chicago. [Read before Chicago Med. Soc, 
Dec. 14, 1898] <Chicago M. Rec, v. 16 (1), Jan., pp. 33-35; discussion, 
pp. 81-83. [Wm.] 

Preston, George J. ; & Ruhrah, John. [M. D.'s, Baltimore City Hosp.] 

1894 a. — Report of a case of amoebic dysentery, with spontaneous cure 
<N. York M. J. (832), v. 60 (19), pp. 593-594. [Wm, Wc] 

von Prowazek, St. [Dr. phil., Wien.] 

1904 1. — Entamoeba buccalis n. sp. Vorlaufige Mitteilung <Arb. a. d. k. 
Gsndhtsamte., Berl., v. 21 (1), pp. 42-44. [Wa, Wm.] 

1910. — Contribuigao para o conhecimento da fauna de protozoarios do Brazil. 
[Portuguese and German text] <Mem. Inst. Oswaldo Cruz, Rio de 
Janeiro-Manguinhos, v. 2 (2), pp. 149-158, figs. 1-3. [MS. dated Apr.] 

1911. — Beitrag zur Entamoeba-Fr&ge <Arch. f. Protistenk., Jena, v. 22 (3), 
pp. 345-350, fig. a, pi. 17, figs. 1-23. [MS. dated Dec. 1910.] [Wa, Wm.] 

1912. — Zur Kenntnis der Entamoba. [Note] <Arch. f. Schiffs- u. Tropen- 
Hyg., Leipz., v. 16 (1), Jan., p. 30. [Wa, Wm.] 

1912.— Entamoeba <Arch. f. Protistenk., Jena, v. 25 (2), pp. 273-274, figs. 
1-6. [MS. dated Juli 1911.] [Wa, Wm.] 


von Prowazek, St. — Continued. 

1912. — Weiterer Beitrag zur Kenntnis der Entamoben. VI <Arch. f. Protls- 
tenk., Jena, v. 26 (2), 22. Juli, pp. 241-249, figs, a-h, pi. 18, figs. 1-28. 
[MS. dated Oct. 1911.] [Wa, Wm.] 
Pru£s, Henri. 

1905. — Dysenterie amibienne et dysenterie bacillaire. Th&se. 115 pp. 8°. 
Toulouse. [Wm.] 
Quincke, H. [Prof., Dr., Kiel.] 

1899 a. — Ueber Protozoen-Enteritis. [Read 4. Aug.] <Berl. klin. Wchnschr., 
v. 36 (46), 13. Nov., pp. 1001-1004, figs. 1-5; (47), 20. Nov., pp. 1032-1035. 
[Wa, Wm.] 
Quincke, H. ; & Ross, Ernst. [Kiel.] 

1893 a.— Ueber Amoben-Enteritis <Berl. klin. Wchnschr., v. 30 (45), 6. 
Nov., pp. 1089-1094, figs. 1-7. [Wa, Wm.] 
Raff, Janet W. [M. Sc] 

1912. — Protozoa parasitic in the large intestine of Australian frogs. Part 2. 
[Read Dec. 14, 1911] <Proc. Roy. Soc. Victoria, Melbourne, n. s., v. 24 
(2), Mar., pp. 343-352, figs. 1-2, pis. 70-71. [Wa.] 
Railliet, Alcide. [Prof., Ecole v6t, Alfort, France.] 

1885 a. — Elements de zoologie m6dicale et agricole. [Fasc. 1], 800 pp., 586 

figs. 8°. Paris. [Published oct.] [Wa.] 
1893 a. — TraitS de zoologie mSdicale et agricole. 2. 6d. [fasc. 1], 736 pp., 
494 figs. 8°. Paris. [Published dec] [Wa.] [For 1. ed., see 1885 a.] 
Rathburn, J. I. [Russell, Ky.] 

1910. — Abscess of the liver; diagnosis and treatment [Read before Ken- 
tucky Med. Ass., Lexington, Sept.] <Kentucky M. J., Bowling Green, 
v. 8 (23), Dec. 1, pp. 2071-2073. [Wm.] 
Raymond, Henry I. [Major, Surg., U. S. Army.] 

1908 a. — Ipecacuanha in amebic dysentery <Mil. Surg., Carlisle, Pa., v. 22 
(1), Jan., pp. 46-54. [Wm.] 
Remouchamps, E. [Dr., Asst., Hoogeschool, Gent.] 

1893 a. — Over een vorm van Amaeoa malariae in Zeeland <Nederl. Tijdschr. 
v. Geneesk., Amst, 2. s., 29. J., v. 2 (24), 16. Dec., pp. 849-854, 1 chart, 
1 pi., figs. A-F. [Wm.] 
Render, Carl D. [M. D., Louisville, Ky.] 

1909. — Clinical diagnosis of amebic dysentery. [Remarks before Ken- 
tucky State Med. Ass., Louisville, Oct. 19-21] < Proctologist, St. Louis, 
v. 3 (4), Dec, p. 259. [Wm.] 
1910. — Clinical diagnosis of amebic dysentery. [Read before Kentucky 
State Med. Ass., Louisville, Oct. 19-21] <Kentucky M. J., Bowling Green, 
v. 8 (1), Jan. 1, pp. 1138-1140. [Wm.] 
Rentsch, S. 

1860 a. — Homoiogenesis. Beitrage zur Natur- und Heilkunde. Erstes 
Heft: Gammarus ornatus und seine Schmarotzer. 1 p. 1., iii+134+31 
pp., 16 pis. 4°. Wismar. [Wm.] 
Rhein, John H. [Dr., Philadelphia, Pa.] 

1892 a.— The Ameba coli <Med. News, Phila., v. 60 (2), Jan. 9, pp. 40-11, 
figs. 1-2. [Wa, Wm.] 
Rho, Filippo. [Dr., Torino.] 

[1894 a]. — La dissenteria e le sue forme rispetto all'amblente soclale, ai 
climi e alle stagioni. Studio eziologico clinico e terapeutlco <Collez. 
ital. dl lett. s. med., Milano, 7. s. (3), pp. 77-131+1 p. (55+1 pp.). 


Rhumbler, Ludwig. [Prof. Dr.; Privatdoc. u. Asst, Gottingen.] 

1898. — Physikalische Analyse von Lebenserscheinungeu der Zelle. 1. 
Bewegung, Nahrungsaufnahme, Defiikation, Vacuoleu-Pulsatlon und 
Gehiiusebau bei lobosen Rhizopoden <Arch. f. Entwcklngsmechn. d. 
Organ., Leipz., v. 7 (1), 6. Sept., pp. 103-350, flgs. 1-100, pis. 6-7, figs. 
A-V. [Wa.] 
1905 c. — Zur Theorie der Oberfliichenkrafte der Amoben <Ztschr. f. 
wissensch. Zool., Leipz., v. 83, 10. Nov., Festschr. Ehlers, v. 2, pp. 1-52, 
flgs. 1-23. [Wa.] 
Riesman. [Dr.] 

1901.— [Discussion of Harris, Henry F., 1901, pp. 191-194] <Proc. Path. 
Soc. Phila., o. s., v. 22, n. s., v. 4 (8), June 1, p. 196. [Wm.] 
Rist, E. 

1907. — Un cas de dysenterie amibienne chronique. (Presentation du 
nialade.) [Read 26 juillet] <Bull. et mem. Soc. m£d. d. h6p. de Par., 
3. s., v. 24 [pt. 2 (27), 1 aug.], pp. 913-915. [Wm.] 
Rivolta, Sebastiano ; & Delprato, Pietro. 

(1881a). — L'ornitoiatria, o la medicina degli uccelli domestic! e senii- 
domestici. Pisa. 
Roberts, Dudley. [M. D.] 

1911. — Observations on the influence of ipecac upon intestinal amoebiasis 
<N. York M. J. [etc.] (1724), v. 94 (25), Dec. 16, pp. 1231-1233. [Wa, 
Roehrig, Clemens. 

1896 a.— Ein Fall von Amoeben-Enteritis. Diss. 22 pp., 1 1. 8°. Kiel. 
Roemer, Friedrich. [Dr. phil., Asst, zool. Inst., Univ. Jena.] 

1898 a. — Amoeben bei Dysenterie und Enteritis <Mtinchen. med. Wchnscbr., 
v. 45 (2), 11. Jan., pp. 41^4, 1 pi., figs. 1-27. [Wm.] 
Roger, G. H[enri]. [Prof, extraord., Fac. med., Paris.] 

1901a. — Introduction to the study of medicine. Authorized translation by 
M. S. Gabriel. With additions by the author, vii+545 pp., flgs. 8°. 
New York. [Wm.] 
Rogers, Leonard. [M. D., Act. Prof., Path., Med. College, Calcutta.] 

1902 m. — Tropical or amoebic abscess of the liver and its relationship to 
amoebic dysentery. [Read before Brit. Med. Ass., July 29-Aug. 1] 
<Brit. M. J., Lond. (2177), v. 2, Sept. 20, pp. 844-851. [Wa, Wm.] 

1903 c— Idem <J. Trop. M., Lond., v. 6 (4), Feb. 16, pp. 58-62; (5), Mar. 2, 
pp. 77-82. [Wa, Wm.] 

1903 s. — Further work on amoebic dysentery in India. The mode of forma- 
tion of secondary amoebic abscess of the liver, with a note on the serum 
test for dysenteries <Brit. M. J., Lond. (2214), v. 1, June 6, pp. 1315-1319, 
figs. 1-5, 1 pi. [Wa, Wm.] 

1905 z. — Blood counts in acute hepatitis and amoebic abscess of the liver, 
with further experience of the relationship of the Amoeba dysenterica to 
tropical liver abscess <Brit. M. J., Lond. (2341), v. 2, Nov. 11, pp. 
1291-1294, 1 table. [Wa, Wm.] 

1907. — The early diagnosis and cure of the presuppurative stage of amoebic 
hepatitis. [Read before Roy. Med. & Chir. Soc] < Practitioner, Lond. 
(468), v. 78 (6); June, pp. 776-790, charts 1-5. [Wm.] 

(1908 a). — Prevention of tropical abscess of the liver by early diagnosis and 
treatment of presuppurative stage of amebic hepatitis <Arch. Int. Med.. 
Chicago, June. 


Rogers, Leonard — Continued. 

1908. — The prevention of tropical abscess of the liver by the early diagnosis 

and treatment of the presuppurative stage of amoebic hepatitis. [Read 

before 5. Ann. Meet. Philippine Islands M. Ass., Feb. 29] <Philippine J. 

Sc, Manila, v. 3 (4), Sept., pp. 285-290, 3 charts. [Wa.] 
190S. — Amoebic abscess of the liver as an easily preventable disease, and 

post-operative sepsis as an important lethal factor. [Read before 76. 

Ann. Meet. Brit. Med. Ass., Sheffield, July] <Brit. M. J., Lond. (2495), 

v. 2, Oct. 24, pp. 1246-1249. [Wa, Wm.] 
1908. — A case of tropical abscess of the liver rapidly cured by means of the 

flexible sheathed trocar <lbidem (2496), v. 2, Oct. 31, pp. 1330-1331, 

1 chart. [Wa, Wm.] 
1909. — The prevention of tropical abscess of the liver by the treatment of 

the presuppurative stage with ipecacuanha <Therap. Gaz., Detroit, v. 33, 

3. s., v. 25 (6), June 15, pp. 381-385. [Wa, Wm.] 
1910. — The prevention and treatment of amoebic abscess of the liver 

<Philippine J. Sc. Manila, v. 5 (2), July, pp. 219-228. [Wa.] 
1912. — The rapid cure of amoebic dysentery and hepatitis by hypodermic in- 
jections of soluble salts of emetine <Brit. M. J., Lond. (2686), v. 1, June 

22, pp. 1424-1425. [Wa, Wm.] 
1912. — Further experience of the specific curative action in amoebic disease 

of hypodermic injections of soluble salts of emetine <Ibidem (2695), 

v. 2, Aug. 24, pp. 405-408. [Wa, Wm.] 
1912. — The rapid and radical cure of amebic dysentery and hepatitis by the 

hypodermic injection of soluble salts of emetine <Therap. Gaz., Detroit, 

v. 36, 3. s., v. 28 (12), Dec. 15. pp. 837-842. [Wa, Wm.] 
Rogers, Leonard; & Wilson, Roger P. 

1906 a. — Two cases of amoebic abscess of liver cured by aspiration and in- 
jection of quinine into the cavity without drainage <Brit. M. J., Lond. 

(2372), v. 1, June 16, pp. 1397-1400, charts 1-2. [Wa, Wm.] 

1912. — Contribution a l'etude de la flore intestinale de l'homme. (Troisieme 

note) : Flore microbienne dans un cas de dysenterie amibienne <Compt. 

rend. Soc. de biol., Par., v. 72 (1). 12 Jan., pp. 25-26. [Wa, Wm, Wc] 
Romano vski. [St. Petersbourg.] 

1908 — Coloration de V Amoeba de la dysenterie <Lavori e riv. di chim. e 

micr. clin., Salsomaggiore (1908-09), v. 1 (1-3), sett.-nov., pp. 25-27. 

Poos, Ernst. [Dr.; Asst.. Med. Klinik, Kiel.] 

1893 a. — Ueber Infusoriendiarrhoe <Deutsches Arch. f. klin. Med., Leipz., 
v. 51 (4-5), 27. Juni. pp. 505-526, figs. 1-7. [Wm.] 

1894 c. — Zur Kenntniss der Amoebenenteritis <Arch. f. exper. Path. u. 
Pharmakol., Leipz.. v. 33 (6L 6. Juli, pp. 389-406, pis. 4-5, figs. 1-9. 
[Wa, Wm.] 

[Rose, Wickliffe.] [Admin. Sec'y, Rockefeller San. Com.] 

1910. — Report of administrative secretary <Publication (3), Rockefeller 
San. Com. Eradication Hookworm Dis., Wash., 38 pp. 15 maps. [Wa, 
Lib. Hassall.] 
Rosenberger, Randle C. [M. D. ; Asst. Prof., Bacteriol., Jefferson Med. College; 
Director, Clin. Lab., Philadelphia Hosp.] 
1911. — The presence of intestinal parasites in patients in the Philadelphia 
General Hospital. [Abstract] <Proc. Path. Soc. Phila., n. s., v. 14 (1), 
Feb., pp. 27-31; discussion, pp. 31-32. [Wm.] 


Rosenberger, Kandle C. — Continued. 

1912. — A case of quadruple Infestation and the occurrence of Amcba in the 
stools of apparently healthy individuals <N. Y >rk If. J. [etc.] (1738), 
v. 95 (12), Mar. 23, pp. 590-591, fig. 1. [Wa, Wm.] 
Rosenthal, L. [Dr.] 

1903. — Zur Aetiologie der Dysenterie. Vorliiuflge Mittheilung < Deutsche 
med. Wclinschr., Leipz., v. 29 (6), 5. Feb., pp. 97-98. [Wa, Wm.] 
Ross, Ronald. 

1897 a. — Notes on some cases of malaria. Amoeba coli and Cercomonas 
<Indian M. Gaz., Calcutta, v. 32 (5), May, pp. 172-175. [Wm.] 
Rousseau, Louis. 

1S33-34 a.— Amine, Amiba <Dict. d'hist, nat., Par., v. 1, p. 137. [VVc] 
Ruffer, Marc Armand [M. A., M. D.] ; & Willmore, J. Graham [Desert Lab., 
El Tor, Sinai]. 
1909.— On the etiology of dysentery <Brit. M. J., Lond. (2543), v. 2, Sept. 
25, pp. 862-866. [Wa, Wm.] 
Ruge, Reinhold. [Dr.; Prof., Univ. Kiel.] 

1901. — Ein Wort zur Behandlung frischer Falle tropischer Dysenterie 
<Deutsche med. Wchnschr., Leipz.. v. 27 (14), 4. Apr., pp. 218-219. 
[Wa, Wm.] 

1903 q. — Zur Aetiologie und Verbreitungsweise der Dysenterie In den 
Tropen. [Author's abstract of paper read before 75. Versamml. deutsch. 
Natnrf. u. Aerzte] <Arch. f. Schiffs- u. Tropen-Hyg., Leipz., v. 7 (12), 
Dec, pp. 571-572. [Wm.] 

1904 f. — Ueber Dysenterie in den Tropen. [Discussion, 23. Sept. 19031 
<Verhandl. d. Gesellsch. deutsch. Naturf. u. Aerzte, Leipz. (75. Ver- 
samml., Cassel, 20.-26. Sept. 1903). 2. Theil, 2. Hiilfte, pp. 489-490. 

1906 b. — Amobenruhr <Handb. d. Tropenkrankh. (Mense), Leipz., v. 3, 

pp. 1-21, figs. 1-7, pis. 1-3. [Wa, Wm.] 
Ruge, Reinhold; & Esau [Dr.]. 

1908 a. — Das Durchwandern der Dysenterie-Amoben dmvh die Darmwand 

<Centralbl. f. Bakteriol. [etc.], Jena, 1. Abt.. v. 46 (2), 3. Feb., Orig., 

p. 129, pis. 1-2, figs. 1-7. [Wa, Wm.] 

Rutherford, Henry H. [First Lieut.; Asst. Surg., U. S. Army.] 

1903 a. — Intestinal diseases <Rep. Surg. -Gen. Army, Wash., pp. 73 77. 
[Wa. Wm.] 
Sakharov, V. N. [Tiflis.] 

1892 a. — Amaeuae malariae (hominis) . Specierum variaruin icones micro- 
photographicae. 1 1., 10 pis. 8°. Tiflis. [Wm.] 

Sambon, Louis Westerna. [M. D. ; Lecturer, London School Trop. Med.] 

1908. — [Tropical abscess of liver.] [Abstract of discussion before 76. Ann. 

Meet. Brit. Med. Ass., Sheffield. July] <Brit. M. J., Lond. (2495), v. 2, 

Oct. 24, p. 1253. [Wa, Wm.] 
Sandwith, Fleming M. [M. D., F. R. C. P.; Prof., Med.. Cairo.l 

1902 a. — [Discussion on dysentery. 10.] [Before Sect. Trop. Dis., Brit. 

Med. Ass., Manchester, July 29-Aug. 1] <Brit. M. J., Lond. (2177), v. 2, 

Sept. 20, p. 852. [Wa, Wm.] 
1908. — [Tropical abscess of liver.] [Abstract of discussion before 76. Ann. 

Meet. Brit. Med. Ass., Sheffield. July] <Ibidem (2495). v. 2, Oct. 24, 

p. 1253. [Wa, Wm.] 


Sntterthwaite, Thomas E. [M. D. ; Path., St. Luke & Presbyterian Hospitals, 
New York.] 
1881 b. — Intestinal parasites <Cycl. Pract. M. (Ziemssen), N. Y., Suppl., 
pp. 217-223, 1 fig. [Wm.j 
Saundby, Robert [M. D., LL. D., F. R. a P.; Senior Phys., Birmingham Gen. 
Hosp.] ; & Miller, James [B. Sc, M. D., M. R. C. P.; Path, to Hosp.]. 
1909 a. — A case of amoebic dysentery with abscess of the liver in a patient 
who had never been out of England <Brit. M. J., Lond. (2517), v. 1, 
Mar. 27, pp. 771-773, 2 pis., figs. 1-9. [Wa, Wm.] 
Saunders, M. B. [Dr.] 

1909 a. — Treatment of amoebic infection <Med. Rec, N. Y. (1998), v. 75 
(8), Feb. 20, p. 315. [Wa, Wm.] 
Say, William J. [Dr.] 

1902.— [Discussion of Nietert, H. L , 1902, pp. 55-61] <St. Louis Med. Rev. 
(1091), v. 46 (4), July 26, p. 65. [Wm.] 
Schaeffer, Charlotte M. [M. D. ; Path. Interne, Sealy Hosp., Galveston, Texas.] 
1901a. — Ancliylo stoma duodenal e In Texas <Tr. Texas M. Ass., Austin 
(Galveston, Apr. 23-26). v. 33. pp. 399-406; discussion, pp. 406-408. 
1901b.— Idem <Med. News. N. Y.. v. 79 (17), Oct. 26, pp. 655-658. [Wa, 
Wm, Wc] 
Schardinger, Franz. [Reginientsarzt, Sarajevo, Bosnien.] 

1896 a. — Reinkulturen von Protozoen auf festen Nahrboden <Centralbl. f. 
Bakteriol. [etc.], Jena, 1. Abt, v. 19 (14-15), 25. Apr., pp. 538-545, figs. 
1-8. [MS. dated Marz.] [Wa, Wm.] 
1897a. — Protozoenkulturen. Nachtrag <Ibidem, v. 22 (1), 20. Juli, pp. 

3-5, pis. 1-2, figs. 1-4. [MS. dated Apr.] [Wa, Wm.] 
1899 a. — Entwicklungskreis einer Amoeba lobosa (Gymnamoeba) : Amoeba 
gruberi <Sitzungsb d. k. Akad. d. Wissensch., Wien, math.-naturw. 
CI, v. 108, 1. Abt. (9), pp. 713-734, pis. 1-2, figs. 1-8. [Wa.] 
Sohaudinn, Fritz. [Prof., Zool. Inst Berlin.] 

1896 b. — Ueber den Zeugungskreis von Paramoeba eilhardi n. g. n. sp. 
<Sitzungsb. d. k. preuss. Akad. d. Wissensch. zu Berl., 1. Halbbd. (2-3), 
23. Jan., pp. 31-41. figs. 1-12. [Wa, Wc] 
1903 a. — Untersuchungen fiber die Fortpflanzung einiger Rhizopoden. 
(Vorlaufige Mittheilung) <Arb. a. d. k. Gsndhtsamte., Berl., v. 19 (3), 
pp. 547-576. [MS. dated 20. Dec 1902 ] [Wa, Wm.] 
Schepotieff, Alexander. [Dr.] 

1910. — Amobenstndien <Zool. Jahrb . Jena, Abt. f. Anat., v. 29 (4), pp. 
485-526, pi. 39, figs. 1-65. [Wa, Wm.] 
Sr*hneidemuehl, Georg. [Prof. Dr., Univ. Kiel.] 

1896 a. — Lehrbuch der vergleichenden Pathologie und Therapie des Men- 
schen und der Hausthiere fur Thierarzte. Arzte und Studirende. 2. Lief., 
pp. 209-448. 8°. Leipzig. [Wa] 
Schneider, Aim£-C.-J. 

1875 f.— Contributions a l'histoire des? gregarines des invert£br£s de Paris 
et de Roscoff <Arch. de zool. expSr. et gen., Par., v. 4 (3), pp. 493-604, 
pis. 16-23. [Wm, Wc] 

1876 n. — Contribution A. l'etude des gregarines. Diss. 116 pp., pis. 16-23. 
8°. Paris. [ Same as 1 875 f . ] [Wa 

Schneider, J. E. J. [Dr., M6d.-major.] 

1908 a. — A propos de la dysenteric amlbienne. [Read 12 fev.] <Bull. Soc 
de path, exot., Par., v. 1 (2), pp 77-78. [Wm.] 


Schneider, Karl Caraillo. [a. o. Prof., Univ. Wien.] 

1905 a. — Plasmastruktur und -bewegung bei Protozoen und Pflanzenzellen 
<Arb. a. d. zool. Inst. d. Univ. Wien [etc.], v. 16 (1), pp. 99-216 
(118 pp.), pis. 1-4. [Ws.] 
Schouteden, H. [Dr., Bruxelles.] 

1905 a. — Notes sur quelques amibes et choanoflagellates <Arcb. f. Pro- 
tistenk., Jena, v. 5 (3), pp. 322-338, figs. 1-12. [Wa, Wm.] 
Schuberg, August. [Dr.; Prof., Zool. k. Gsndhtsamte., Berlin.] 

1893 n. — Die parasitischen Amoeben des menschlichen Darmes. Kritische 
Uebersicht ueber die Entwickelung und den gegenwaertigen Stand 
unserer Kenntnisse <Centralbl. f. Bakteriol. [etc.], Jena, v. 13 (18-19), 
4. Mai, pp. 598-609; (20), 17. Mai, pp. 654-665; (21-22), 29. Mai, pp. 
701-714. [Wa, Wm, Wc] 
Schubert, Max. 

1897 a. — Ueber die Ziichtung der Amoben auf festen N&hrboden <Hyg. 
Rundschau, Berl., v. 7 (2), 15. Jan., pp. 72-76. [Wa, Wm.] 
Schubotz, Hermann. 

1905 a. — Beitriige zur Kenntnis der Amoeba blattae (Btitschli) und Amoeba 

proteus (Pall.). Diss. 46 pp., 1 1., 2 pis. 8°. Jena. [Wc] 
1905 b.— Idem [?] <Arch. f. Protistenk., Jena, v. 6 (1), pp. 1-46, pis. 1-2. 
[Wa, Wm.] 
Scott, J. Alison. [M. D.] 

1901. — Amebic abscess of liver <Proc. Path. Soc. Phila., o. s., v. 23, n. s., 
v. 5 (1), Nov., pp. 11-15. [MS. dated Oct. 24.] [Wm.] 
Scott, William. [M. D., Loveland, Ohio.] 

1912. — Amebic dysentery. [Read before Warren Co. Med. Soc, Lebanon, 
O., June] <Lancet-Clinic, Cincin., v. 108 (2), July 13, pp. 39-41. [W T m.] 
Seaman, William. [M. D. ; Surg., U. S. Navy.] 

1911. — The surgical treatment of amebiasis. [Read at 8. Ann. Meet Am. 
Soc. Trop. Med., N. Orl., May 18-19] <N. Orl. M. & S. J., v. 64 (2), 
Aug., pp. 105-110. [Wm.] 
Seifert, Otto. [Prof. Dr., Wtirzburg.] 

1908 a.— Klinisch-therapeutischer Teil. pp. [477]-623. 8°. Wiirzburg. 
[Anhang to Braun, Max., 1908, 475 pp.] [Wa.] 
Selenev, I. F. 

1909. — Dermatitis desquamativo-pustulosa amoebina. [Abstract from Rus- 
sische Ztschr. f. Haut- u. Geschlechtskrankh.. Juni, 1908, by A. Dwo- 
retzky] <Hyg. Rundschau, Berl., v. 19 (9), 1. Mai, p. 549. [Wa, Wm.} 
Sellards, Andrew Watson. 

1911. — Immunity reactions with amoebae <Phllippine J. Sc, Manila, B : 
Med. Sc, v. 6 (4), Oct., pp. 281-298. [Wa.] 
Shaw, Frank Whitfield. [Dr.] 

1901. — Parasites, animal and vegetable <Diagn. Intern. Med. (Butler), 

N. Y., pp. 600-603, figs. 217-218; pp. 619-621, figs. 220-221. [Wm.] 
1905. — Parasites, animal and vegetable <Ibidem, N. Y. & Lond., 2. ed.. pp. 

641-644, fig. 256; pp. 662-664, figs. 261-262. [Wm.] 
1909. — Parasites, animal and vegetable <Ibidem, 3. ed., pp. 654-657. figs. 
256-257; pp. 679-S81, figs. 261-262. [Wm.] 
Shiga, K. [Dr.; Asst, Inst. Infektionskr., Japan.] 

1898. — Ueber den Dysenteriebacillus (Bacillus dysenteriae) <Centralbl. 1 
Bakteriol. [etc.], Jena, 1. AM., v. 24 (22), 15. Dec, pp. 817-828, figs. 1-4; 
(23), 19. Dec, pp. 870-874; (24). 23. Dec, pp. 913-918. [MS. dated Dec 
1897.] [Wa, Wm.] 


Shiga, K. — Continued. 

1901. — Studien iiber die epidemische Dysenterie in Japan, unter besonderer 
Beriicksichtigung des Bacillus dysenteriae <Deutsche rned. Wchnschr., 
Leipz., v. 27 (43), 24. Oct., pp. 741-744; (44), 31. Oct., pp. 765-769, charts 
1-7; (45), 7. Nov., pp. 783-786, 1 fig. [MS. dated Marz.] [Wa, Wm.] 
1902 a. — Bemerkungen zu Jager's " Die Ostpreussen einheiinische Ruhr, 
eine Amoben-Dysenterie " <Centralbl. f. Bakteriol. [etc.], Jena, 1. Abt, 
v. 32 (5), 5. Sept., Orig., pp. 352-353. [Wa, Wm.] [See Jaeger, H.. 
1902 g.] 
Shipley, Arthur Everett. [M. A.; Hon. D. Be. ; Princeton, F. R. S. ; Fellow 
Tutor, Christ's College, Cambridge, England.] 
[1908 d.] — Interim report on the parasites of grouse. 12 pp. fol. [Lon- 
don.] [MS. dated July.] [Wa.] 
Short, Alfred Terry. [M. D. ; Police Surg., Manila, P. I.] 

1905. — Note on tropical dysentery <J. Ass. Mil. Surg. U. S., Carlisle, Pa., 
v. 17 [(3), Sept.], pp. 211-212. [Wm.] 
von Siebold, Carl Theodor Ernst. [Prof., Freiburg i. Breisgau.] 

[1850 c]. — Parasiten <Handworterb. d. Physiol.. Brnschwg., v. 2, pp. 
641-692. [Wm.] 
Siler. Joseph F. ; & Nichols, Henry J. [Captains, Med. Corps, U. S. Army.] 

1909. — Observations on pellagra at the Peoria State Hospital, Peoria, 111. 
<Bull. Illinois State Bd. Health, Springfield, v. 5 (7), Oct., pp. 437-478. 
figs.; (8), Nov., pp. 48a- [572], figs. [Wa] 
1910. — Observations on pellagra at the Peoria State Hospital, Peoria, III. 
<Med. Rec, N. Y. (2045), v. 77 (3), Jan. 15, pp. 87-98. [Wa, Wm.] 
de Silvestri, Enrico. [Dr.] 

1895. — Contributo alio studio dell' etiologia della dissenteria. [Read 21 
die. 1894] <Gior. r. Accad. di med. di Torino, an. 58, 4. s., v. 1 (1), 
genua io, pp. 32-36. [Wm.] 
Simon, Charles Edmond. [M. D. ; Late Asst. Resident Physician, Johns Hop- 
kins Hosp., Baltimore ,Md.] 
1890 a. — Abscess of the liver, perforation into the lung; Amoeba coli in 
sputum. [Abstract of paper read before Johns Hopkins Hosp. Med. Soc, 
Oct. 6] < Johns Hopkins Hosp. Bull., Bait., v. 1 (8), Nov.. p. 97. [Wm, 

1896 a. — A manual of clinical diagnosis by means of microscopic and chemical 
methods, for students, hospital physicians, and practitioners. xix+[17]- 
504 pp., 132 figs., 10 pis. 8°. Philadelphia & New York. [Wm.] 

1897 a. — Idem. 2. ed., revised and enlarged, xx-f [17]-563 pp., 133 figs., 
14 pis. 8°. Philadelphia & New York. [Wm.] 

[1900 a]. — Idem. 3. ed., thoroughly revised, xxiv+17-558 pp., 136 figs., 
18 pis. 8°. Philadelphia & New York. [Wm.] 

[1904 a]. — Idem. 5. ed., thoroughly revised and enlarged. xxiv-f-17-695 
pp., 150 figs., 22 pis. 8°. Philadelphia & New York. [Wa, Wm.] 

1907.— Idem. 6. ed., thoroughly revised. xix+[17]-682 pp., 177 figs., 24 
pis. 8°. Philadelphia & New York. [Wa.] 

[1911]. — A manual of clinical diagnosis by means of laboratory methods for 
students, hospital physicians, and practitioners. 7. ed., enlarged and 
thoroughly revised, xviii + 17-778 pp., 168 figs., 25 pis. 8°. Philadel- 
phia & New York. [Wa.] 
Simon, Sidney K. [A. B., M. D. ; New Orleans, La.] 

1909. — Amebic dysentery. [Read before 6. Ann. Sess. Am. Med. Ass., At- 
lantic City, June] <J. Am. M. Ass., Chicago, v. 53 (19), Nov. 6. pp. 1526- 
1529; discussion, pp. 1529-1532. [Wa, Wm.] 


Simon, Sidney K. — Continued. 

1910.— Treatment of dysentery <N. Orl. M. & S. J., v. 63 (3), Sept., pp. 

193-199; discussion, pp. 199-201. [Wm.] 
1912.— A further word on the ipecac treatment of amebic dysentery <N. 
Orl. M. & S. J., v. G5 (5), Nov., pp. 373-377 ; discussion, pp. 377-379. [Wm.] 
Sistrunk, W. E. [M. D. ; Asst. Path., Gen. Lab., St. Mary's Hosp., Rochester, 
1911. — Intestinal parasites found in individuals residing in the northwest. 
Frequent presence of Protozoa in patients who have never been in 
southern countries <J. Am. M. Ass., Chicago, v. 57 (19), Nov. 4, pp. 1507- 
1509. [Wa, Wm, Wc] 
Skshivan, F. F. ; & Stefauski, V. K. 

1908. — K voposu ob etiologii dizenterii v Rossii. 6 sluchaev amebnoi 
dizenterii v. Odessie < Kharkov. M. J., v. 5 (4), Apr., pp. 371-385. 
Slaughter, R. M. [M. D., Theological Seminary, Va.] 

1895 a. — Abscess of the liver in children, with report of a case of amoebic 
abscess < Virginia M. Month., Richmond (259), v. 22 (7), Oct., pp. 
722-731. [Wa, Wm.] 
Sluiter, C. Ph. [Dr., Hoogleeraar, Univ. v. Amsterdam] ; & Swell engrebel, N. H. 
[Dr., Privat-Doc, Univ. v. Amsterdam]. 
1912. — De dierlijke parasieten van den mensch en van onze huisdieren. 
Tweede veel vermeerdede en verbeterde druk. xvi+520 pp., 262 figs., 1 pi. 
8°. Amsterdam. [Wm.] 
Smith, Allen J. [M. D. ; Prof., Path., Univ. Penn., Philadelphia, Pa.] 

1901. — A previously described spore-forming bacillus associated with the 
Ameba coli in hepatic abscess <Tr. Texas M. Ass., Austin (33. Ann. Sess., 
Galveston, Apr. 23-26), pp. 409-412. [Wm.] 
1911. — [Discussion of Rosenberger, Randle C, 1911, pp. 27-31] <Proc. 
Path. Soc. Phila., n. s., v. 14 (1), Feb., pp. 31-32. [Wm.] 
Smith, Allen J. ; & Magnenat, L. E. [Demonstrator, Norm. Histol., Med. Dept^ 
Univ. Texas, Galveston, Texas]. 
1898. — Amoeba coli and actute cystitis <Internat. M. Mag., Phila., v. 7 (4), 
Apr., pp. 253-255. [Wm.] 
Smith, Allen J. ; & Weidman, F. D. 

1910. — Infection of a stillborn infant by an amebiform protozoon {Enta- 
moeba mortinatalium, n. s.) <Univ. Penn. M. Bull., Phila., v. 23 (5-6), 
July-Aug., pp. 285-298, figs. 1-19. [Wa, Wm.] 
1910. — Supplementary note to article upon Entameba met in a stillborn 
infant, in last month's issue of the University of Pennsylvania Medical 
Bulletin <Univ. Penn. M. Bull., Phila., v. 23 (7), Sept., pp. 359-360. 
[MS. dated Aug. 19.] [Wa, Wm.] 
Smith, Rea. [M. D., Los Angeles, Calif.] 

1912. — A report of twenty-eight cases of tropical abscess of the liver. 
[Read before 42. Ann. Meet., State Soc, Del Monte, Apr.] <Calif. State 
J. M., San Fran., v. 10 (7), July, pp. 300-302; discussion, pp. 302-303. 
Smith, R. J. [M. D., Smithfield, Utah.] 

1906. — Treatment of amebic dysentery <Northwest Med., Seattle, v. 4 
(12), Dec, pp. 420-422. [Wm.] 
Smith, Theobald. [M. D. ; Prof., Harvard Univ., Cambridge, Mass.] 

1895 a. — An infectious disease among turkeys caused by Protozoa (infec- 
tious entero-hepatitis) <Bull. 8, Bureau Animal Indust., U. S. Dept. 
Agric, Wash., pp. 1-38, pis. 1-5. [Wa, W T c] 
66692— vol 2, pt 1—13 17 


Smith, Theobald — Continued. 

1910. — Amoeba meleagridis. [Letter to editor, dated Sept. 20] < Science, 

N. Y., n. s. (824), v. 32, Oct. 14, pp. 509-512. [Wa, Wm, Wc] 
1910. — Intestinal amebiasis in the domestic pig <J. Med. Research, Bost. 
(123), v. 23, n. s., v. 18 (3), Nov., pp. 423-432, pis. 16-17, figs. 1-5. 
[Wa, Wm.] 
Sominer, Ferdinandus Bernardus Guilelmus. [Prof., Director d. anat. Inst, 
1880 b. — Amoeba coli (Losch) <Real-Encycl. d. ges. Heilk., Wien & Leipz., 

v. 1 (4-5), pp. 246-247, fig. 30. [Wm.] 
1893 a.— Amoeba coli (Losch) <Ibidem, 3. Anfl. (7-8), v. 1, pp. 497-499, fig. 
53. [Wm.] 
Sonsino, Prospero. [Prof., Pisa.] 

1896 a. — Contributo alia entozoologia d'Egitto <M£m. de l'lnst. egypt, Le 
Caire, v. 3 (3), pp. 285-336. [Wa.] 

Spalikowski, Ed. 

1897 a. — Les entozoaires de l'homme en Normandie <Compt. rend. Acad. d. 
sc, Par., v. 125 (24), 13 dec, pp. 1056-1057. [Wa, Wm, Wc] 

Spelman, J. P. ; & Wherry, William B. 

1906 a. — A case of amebic dysentery, originating in Montana. A case of 
latent malaria. [Read before Montana State Med. Ass., May] <North- 
west Med., Seattle, v. 4 (8), Aug., pp. 277-279. [Wm.] 
Steele, J. D. [Dr.] 

1896. — Amoebic abscess of liver. [Specimens exhibited & remarks, Nov. 8, 
1894] <Tr. Path. Soc Phila. (1893-95), v. 17, pp. 38-39. [Wm.] 
Steffenhagen, Karl. 

1903 a. — Ueber einen Fall von Amobendysenterie mit sekundarem Leber- 
abscess. Diss. 34 pp., 1 1. 8°. Munchen. [Wm.] 

(1862 a). — Ueber die auf und zwischen den menschlichen Zahen sich 
ansammelnde weisse Substanz <Ztschr. f. neuere Med., Kiew. 
Stengel, Alfred. [M. D. ; Instructor, Clin. Med., Univ. Penn., Philadelphia, Pa.] 

1890 a.— Acute dysentery and the Amoeba coli <Med. News, Phila. (931), 
v. 57 (20), Nov. 15, pp. 500-503, figs. 1-3. [Wa, Wm.] 

1891.— Amoeba coli. [Remarks, May 23] <Tr. Path. Soc. Phila. (1889-91), 
v. 15, pp. 99-101 ; discussion, pp. 101-102. [Wm.] 

1891b. — The Amoeba coli <Univ. M. Mag., Phila., v. 4 (3), Dec, pp. 218- 
224, figs. 1-3. [Wm.] 

1892 a.— Idem [continued] <Ibidem, v. 4 (4), Jan., pp. 286-293. [Wm.] 

1898.— Amebic abscess of the liver. [Read Jan. 28, 1897] <Tr. Path. Soc 
Phila. (1895-97), v. 18, pp. 103-110. [Wm.] 
Stephens, J. W. W. [M. D.] 

1909.— Cultures of Amoeba. [Read Sept. 8, 1908] <Rep. Brit. Ass. Adv. Sc, 
Loud. (78. Meet, Dublin, Sept. 1908), Tr. of Sect, p. 741. [Wa.] 
Stiles, Charles Wardell. [A. B., Ph. D., D. Sc. ; Prof., Zool., Hyg. Lab., U. S. 
Pub. Health & Mar.-Hosp. Serv., Washington, D. C] 

1902 hh. — The significance of the recent American cases of hookworm dis- 
ease (uncinariasis or auchylostomiasis) in man <18. Ann. Rep. Bureau 
Animal Indust, U. S. Dept Agric, Wash. (1901), Dec. 18, pp. 183-219, 
i\zs. 113-196 [Wa, Wm, Wc] 

l!X)5e— Report of the committee on the relation of Protozoa to disease: In 
particular "Amoeba coli" <Pai>ers & Rep. Am. Pub. Health Ass., Colum- 
bus, O., v. 30, pp. 292-303. [Wm.] 


Stiles, Charles Wardell — Continued. 

1007 e. — The zoo-parasitic diseases of man. (Exclusive of protozoan infec- 
tions) Olodern Med. (Osier), Phila. & N. Y., v. 1, pp. 525-037, tiga 
35-G8, pi. 9. [Wa, Win.] 

1911. — The presence of Entamoeba histolytica and E. coli in North Carolina. 
<Puh. Health Rep., U. S. Pub. Health & Mar.-Hosp. Serv., Wash., v. 28 
(34), Aug. 25, p. 1276. [Wa, Win.] 

1911 — The presence of Lamblia duodcnalis in man in North Carolina and 
the recognition of Amcbac in feces several days old <Pub. Health Rep., 
U. S. Pub. Health & Mar.-Hosp. Serv., Wash., v. 26 (36), Sept. 8, pp. 
1347-134S. [Wa, Wm.] 
Stiles, Charles Wardell; & Hassall, Albert [Asst. Zool., Bureau Animal Indust., 
U. S. Dept. Agric, Washington, D. C] 

1910b. — Compendium of animal parasites reported for rats and mice (genua 
Mus) <[Pub. Health Bull.], U. S. Pub. Health & Mar.-Hosp. Serv., Wash., 
pp. 111-122. [Wa.] 
Stitt, E R. [A B., Ph. G., M. D. ; Surg., U. S. Army.] 

1909. — Practical bacteriology, blood work and animal parasitology, including 
bacteriological keys, zoological tables and explanatory clinical notes. 
xi+294 pp., 8 blank leaves, 82 figs., 4 pis., 56 figs. 12°. Philadelphia. 
[Wa, Wm.] 

1910. — Idem. 2. ed., revised and enlarged, xiii-f-345 pp., 8 blank leaves, 
87 figs., 4 pis., 56 figs. 12°. Philadelphia. [Wa.] 

1911. — Case of amoebic dysentery with liver abscess <U. S. Naval Med. 
Bull., Wash., v. 5 (2), Apr., p. 180. [Wa.] 
Stockton, Charles C. [M. D. ; Prof., "Med., Univ. Buffalo; Attend. Physician, 
Buffalo Gen. Hosp.] 

1S94. — Amoebic dysentery. Clinical lecture delivered at the Buffalo Gen- 
eral Hospital <Internat. Clin., Phila., 4. s., v. 1, pp. 69-73. [Wm.] 
Storck, J. A. [M. Ph., M. D., New Orleans, La.] 

1911. — The copper salts and ipecacuanha in the treatment of amebic colitis. 
A comparative study. [Read before Louisiana State Med. Soc, 1910] 
<N. Ory. M. & S. J., v. 63 (11), May, pp. 775-781. [Wm.] 
Streett, David. [M. D. ; Prof., Prin. & Pract. Med. & Clin. Med., Baltimore MeoL 

1893. — Amoeba coli; or the report of a case of amoebic dysentery. [Read 
before Baltimore Med. Ass., Nov. 12] <Maryland M. J., Bait. (661), v. 
30 (5), Nov. 25, pp. 92-99. [Wm.] 
Strong, Lawrence Watson. [M. D., Second Asst. Path., Boston City Hosp.] 

1898 a. — Two cases of amoebic enteritis <Med. & Surg. Rep. Bost. City 
Hosp., 9. s., pp. 249-259. [Wm.] 
Strong, Richard P. [Dr.; Chief, Biol. Lab., Bureau Science, Manila, P. I.] 

1901 c. — The etiology of the dysenteries of the Philippine Islands <Circ. 
Trop. Dis., Manila (2), Apr., pp. 1-54. [Wm.] 

1901 e. — Board for the investigation of tropical diseases in the Philippines- 
Circular No. 1. Animal parasites <Rep. Surg.-Gen. Army, Wash., pp. 
203-219. [Wm.] 

1901. — Idem <Ann. Rep. War Dept, Wash., v. 1, pt 2, Bureau Rep., pp. 
741-757. [Wa, Wm.] 

1905 b. — Intestinal hemorrhage as a fatal complication in amoebic dysen- 
tery and its association with liver abscess. 1 < [Publication] (32), 
Bureau Govt. Lab., Manila, June, pp. 1-15. [Wa, Wm.] 

1907 a. — Amoebic dysentery Olodern Med. (Osier), Phila. & N. Y., v. L 
pp. 488-524, pis. 5-8. [Wa, Wm.] 


Strong, Richard P. ; & Musgrave, William E. 

1900 a. — Preliminary note regarding the etiology of the dysenteries of 
Manila <Rep. Surg.-Gen. Army, Wash., pp. 251-273. [Wa, Win.] 
Sullivan, William Noibert. [M. D., San Francisco, Calif.] 

1900 a. — Colostomy for the cure of amebic dysentery < J. Am. M. Ass., 
Chicago, v. 35 (23), Dec. 8, pp. 1475-1476. [Wm, Wc] 
Swellengrebel, N. H. [Dr.; Privatdoz., Univ. Amsterdam.] 

1910. — Notiz uber eine neue freilebende Amobe Amoeba salteti n. sp. 
<Arch. f: Protistenk., Jena, v. 19 (2), pp. 167-177, pis. 5-6, figs. 1-50. 
[MS. dated 2. Marz.] [Wa, Wm.] 
Takamiya, T. [Staff Surgeon.] 

1912. — Two cases of amoebic dysentery <Bull. Naval M. Ass. Japan, Tokyo 
(1), May, pp. [1-6] ; abstract, p. 5. [Naval Med. School Lib.] 
Talamon, Ch. 

1891 b.— Amibes de la dysenterie <Med. mod., Par., v. 2 (30), 23 juillet, 
pp. 550-552. [Wm.] 
Tanaka, Y. [Dr.] 

1903. — Pathologische Studien uber die Amoebendysenterie. (1. Mittheil- 

ung.) Histologische Untersuchungen uber die Beziehung der Amoeba 

colt zur dysenterischen Darmveranderung. [Japanese text] <Chu-gai 

Iji-Shimpo, Tokio, v. 23 (11), 5. Juni, pp. 1-29. [Wm.] 

(1903 a). — [Vacuoles of Ameba in dysenteric stools.] [Japanese text] 

<Iji Shinbun, Tokio (649), Nov., p. 1619. [Wm.] 
1905 a. — Ueber die Vakuolen der Amoben im dysenterischen Sluhl. [Ab- 
stract of 1903 a, by K. Miura] <Oentralbl. f. Bakteriol. [etc.], Jena, 1. 
Abt, v. 37 (1-3), 2S. Aug., Ref., p. 68. [Wa, Wm.] 
1910. — Bemerkungen iiber die Pathogenitat der Amoeba dysenteriae <Miin- 
chen. med Wchnschr., v. 57 (44), 1. Nov., pp. 2300-2301. [Wa, Wm.] 
Tayler- Jones, Louise. [M. D., Washington, D. C] 

1904. — Dysentery. A report of several cases in which Bacillus dysenteriae 
(Shiga) was found in Washington, D. C. [Read before Med. Soc. Dist. 
Columbia, May 11] <J. Am. M. Ass., Chicago, v. 43 (1), July 2, pp. 12-14. 
[Wa, Wm.] 
Taylor, W. H. [M. D., Central Mills, Alabama.] 

1903 a. — Amebic dysentery. Report of a case <Alabama M. J., Birmingh., 
v. 16 (1), Dec, pp. 10-13. [Wm.] 
Thayer, Alfred Edward. [M. D. ; Prof., Path., Univ. Texas.] 

1907 a.— Study of a case of yellow fever <Med. Roc, N. Y. (1888), v. 71 
(2), Jan. 12, pp. 45-49, figs. 1-2. [Wa, Wm, Wc] 
Thayer, William Sydney [M. D. ; Prof., Med., Johns Hopkins Hosp., Baltimore, 
Md.] ; & Flexner, Simon. 
1893 a. — Demonstration of specimen of amoebic abscess of liver. [Rend 
before Johns Hopkins Hosp. Med. Soc, Mar. 20] <Johns Hopkins Hosp. 
Bull., Bait, v. 4 (31), May, pp. 56-58. [Wa, Wm, Wc] 
Thomas, Jerome B. [M. D., Baguio, Benguet, P. I.] 

1905 a. — The action of various chemical substances upon cultures of 
amoebae < [Publication] (32), Bureau Govt. Lab., Manila, June, pp. 17- 
29. [Wa, Wm.] 

1906 a. — Report on the action of various substances on pure cultures of the 
Ameba dysenteriae <Am. J. M. Be, Phila. & N. Y., n. s. (406), v. 131 (1), 
pp. 108-118. [Wm.] 

Thornburgh, Robert M. [Capt., Asst. Surg., U. S. Army.] 

l*M)Sa. — The treatment of amebic dysentery <Mil. Surg., Carlisle, Pa., v. 22 
(1), Jan., pp. 55-59. [Wm.] 


Tietze, Alexander. [Prof. Dr., Breslau.] 

1905 a. — Ein Prolozoenbefund in einer erkrankten Parotis <Mitt. a. d. 
Grenzgeb. d. Med. u. Chir., Jena, v. 14 (3), pp. 303-310, pi. 7. [Win. J 
Trible, G. B. [Passed Asst. Surg., U. S. Navy.] 

1911. — Lamblia intcstinalis and Axcaris lumbricoidcs associated with amoe- 
bic dysentery <U. S. Naval Med. Bull., Wash., v. 5 (2), Apr., pp. 178- 
180. [Wa, W T m.] 
1911. — Balantidium coli infection associated with amoebic dysentery < Ibi- 
dem (3), July, pp. 346-548. [Wa, Wm.] 
Tsujitani, J. 

1898 a. — Ueber die Reinkultur der Amoben <Centralbl. f. Bakteriol. [etc.], 
Jena, 1. Abt, v. 24 (18-19), 18. Nov., pp. 666-670. [Wa, Wm.] 
Turck, Fenton B. [Dr., Chicago, 111.] 

1909. — [Discussion of Bates, John Pelham, 1909, pp. 56-59] <J. Tennessee 
State M. Ass., Nashville, v. 2 (2), June, p. 60. [Wm.] 
Tuttle, James P. [M. D. ; Prof., Rectal Surgery, New York Policlinic] 

1903 a. — Local lesions and treatment of amebic dysentery. [Secretary's 
abstract of paper read before 29. Meet. Miss. Valley Med. Ass., Memphis, 
Tenn., Oct. 7-9] <Med. News, N. Y. (1606), v. 83 (17), Oct. 24, p. 812. 
[Wa, Wm, Wc] 

1904 a. — Amebic dysentery. Its local lesions and treatment. [Read before 
55, Ann. Sess. Am. Med. Ass., June 7-10] <J. Am. M. Ass., Chicago, 
v. 43 (15) , Oct. 8, pp. 1022-1026 ; discussion, pp. 1026-1027. [Wa, Wm, Wc] 

1904 b.— Idem <Alabama M. J., Birmingh., v. 16 (11), Oct., pp. 561-571; 

discussion, pp. 571-573. [Wm.] 
1905. — Local lesions and treatment of amebic dysentery. [Read before 

Mississippi Valley Med. Ass., Memphis, Tenn., Oct. 7-9, 1903] <Lancet- 

Clinic, Cincin., v. 94, n. s., v. 55, Sept. 23, pp. 348-353; discussion, pp. 

353-356. [Wm.] 
1909.— [Discussion of Simon, Sidney K., 1909, pp. 1526-1529] <J. Am. M. 

Ass., Chicago, v. 53 (19), Nov. 6, p. 1531. [Wa, Wm, Wc] 
Ucke, A. [Prosector, deutsch. Alexanderhospital f. Manner, St. Petersburg.] 
1902 a. — Zur Verbreitung der Amobenenteritis <Centralbl. f. Bakteriol. 

[etc.], Jena, 1. Abt., v. 31 (7), 12. Marz, Orig., pp. 317-318. [MS. dated 

Dec. 1901.] [Wa, Wm, Wc] 

1903.— [Discussion of Huber, J. Ch., 1903 b] < Deutsche med. Wchnschr., 

Leipz., v. 29 (34), 20. Aug., Ver.-Beilage, p. 267. [Wa, Wm.] 
Upiavici, O. [Dr.] 

(1887 a). — Piedbezne sdeleni <Casop. lek. cesk., v Praze. 

1887 b.— Idem [reviewed by Kartulis] <Centralbl. f. Bakteriol. [etc], 

Jena, v. 1 (18), pp. 537-539. [Wa, Wm, Wc] 

1887 c. — The amoebae of dysenteric stools. [Editorial abstract] <Lancet, 
Lond. (3334), v. 2, July 23, p. 184. [Wm, Wc] 

1888 a. — Le amebe nelle dejezioni dissenteriche, negli ascessi epatico con- 
secutivi alia dissenteria. [Abstract of 1887 a] <Boll. sclent., Pavla, 
v. 10 (1), mar., pp. 30-31. [Wm, Wc] 

1888 b. — Le amebe nelle dejezioni dissenteriche. [Abstract of 1887 a] 
<Gazz. med. ital. lomb., Milano, v. 48, 9. s., v. 1 (22), 2 giugno, p. 218. 
Vahlkampf, Erich. [Hamburg.] 

(1904 a). — Beitrage zur Biologie und Entwicklungsgeschichte von Amoeba 
Umax einschliesslich der Zuchtung auf kiinstlichen Nahrboden. Diss. 
53 pp., 1 pi. 8°. Marburg. 


Vahlkampf, Erich — Continued. 

1905 a.— Idem <Arch. f. Protistenk., Jena, v. 5 (2), pp. 167-220, pi. 6, 
figs. 1-27. [Wa, Wm.] 

Vaillard, L. ; & Dopter, Ch. 

1903 a. — Contribution a l'etiologie de la dysenteric La dysenterie epi- 
demique <Ann. de l'lnst. Pasteur, Par., v. 17 (7), 25 juillet, pp. 463-491, 
pis. 10-13. [Wa, Wm.] 

Vedder, Edward B. [A. M., M. D. ; Capt, Med. Corps, U. S. Army.] 

1906 a. — An examination of the stools of 100 healthy individuals, with 
especial reference to the presence of Entamoebae coli <J. Am. M. Ass., 
Chicago, v. 46 (12), Mar. 24, pp. 870-872. [Wa, Wm, Wc] 

1907 a. — Is the distinction between Entamoeba coli and Entamoeba dysen- 
teriae valid? <J. Trop. M. & Hyg., Lond., v. 10 (11), June 1, pp. 190-195. 
[Wa, Wm.] 

1911. — A preliminary account of some experiments undertaken to test the 

efficacy of the ipecac treatment of dysentery. [Read before Manila Med. 

Soc, Feb. 6] <Bull. Manila M. Soc, v. 3 (3), Mar., pp. 48-53; discussion, 

pp. 5S-59. [Naval Med. School. -Lib.] 
1912. — [Treatment of amebic dysentery.] [Abstract of 1911, pp. 48-53] 

<West Virginia M. J., Wheeling, v. 6 (10), Apr., p. 344. [Wm.] 
1912. — An experimental study of the action of ipecacuanha on amoebae. 

[Secretary's abstract of paper read before 2. bien. Cong. Far East. Ass. 

Trop. M., Hong Kong] <J. Trop. M. & Hyg., Lond., v. 15 (20), Oct. 15, 

pp. 313-314. [Wa, Wm.] 
Verdun, P. [Prof., zool. med. et pharm. & la Faculte de med. de Lille.] 

1904 a. — Procede de coloration de l'amibe de la dysenterie et des abc£s 
tropicaux du foie. [Read 6 fev.] <Compt. rend. Soc. de biol., Par., v. 56 
(5), 12 fev., pp. 181-182. [Wa, Wm, Wc] 

1904 d. — Sur quelques caracteres specifiques de l'amibe de la dysenterie et 
des abces tropicaux du foie {Amoeba coli Loescb). [Read 6 fev.] 
< Ibidem, pp. 183-185. [Wa, Wm, Wc] 

1904 f. — Quelques apergus sur l'etiologie de la dysenterie <Echo med. du 
nord, Lille (396), v. 8 (33), 14 aoilt, pp. 385-396; (397) (34), 21 aout, 
pp. 397-401; (398) (35), 28 aout, pp. 409-417; (399) (36), 4 sept, pp. 
421-124. [Wm.] 

1905 a.— Precis de zoologie. ii pp., 1 p. 1., 559 pp., 424 figs. 12°. Paris. 

1907 a. — Precis de parasitologie humaine. Parasites animanx et vegetaux 

(les bacteries exceptees) . iii+727 pp., 310 figs., 4 pis. 12°. Paris. [Wa.] 
Verdun, P. ; & Bruyant, L. 

1907 c — Sur la presence d'amibes dans le pus d'abces de la region malairc 

[Read 20 juillet] <Compt. rend. Soc. de biol., Par., v. 63 (26), 26 juillet. 

pp. 161-163. [Wa, Wm, Wc] 
Viereck, H. [Dr., Oberarzt, Inst. Schiffs- u. Tropenkrankh., Hamburg. 1 

1906 c— Ueber Amobendysenterio <Med. Klin., Berk, v. 2 (41), 14. Oct., 

pp. 1063-1066. [Wm.] 
1907 c — Studien fiber die in den Tropen erworbeno Dysenterie (Dysenterie 

tropicale) <P»eihefte z. Arch. L Schiffs- u. Tropen-Hyg., Leipz., v. 11 

(1), Juli, 41 pp., 3 pis. [Wm.] 
Vincent, II. [ Med.-major, l re classc] 

1903 a.-llii cas de dysenterie amibienne <Presse med , Par. (102), 23 dec, 

pp. 879-881, figs. 1-3. [Wm.] 
1907.— [Discussion of Caussade & .Toltrain, 1907. pp. 167-174] [15 fev.] 

<Bull. et nx'in. Soc. nifd. d. hop. de Par., 3. s., v. 24, pp. 174-176. [Wm.] 


Vincent, H. — Continued. 

1908.— [Discussion of Menetrier, P.; & Touraine, A., 1908, pp. 905-913] 

< Ibidem, v. 25, p. 1)14. [Wm.] 
1909 a. — Note sur la latence prolonged de l'aniibe dysent£riquo dans l'intes- 
tin Domain, Les " porteurs d'amibes " <Bull. Soc. de path, exot, Par., 
v. 2 (2), 10 fev., pp. 78-80. [Wm.] 
1909 c. — Emploi de l'hypochlorite de soude pour le traitement de la dysen- 
terie amibienne cbroni(pie <Bull. Soc. de path, exot., Par., v. 2 (2), 10 
fev., pp. 80-83. [Wm.] 
Vivaldi, Michelangelo. [Dr.] 

1894 a. — Le amebe nella dissenteria <Riforma med., Napoli, an. 10 (238). 
v. 4 (13), 15 ott, pp. 147-149. [Wm.] 
Vollbracht. [Dr.] 

1904 a. — Amoebenenteritis. [Read before Gesellsch. f. innere Med. u. 
Kinderb., Wien, 9. Juni] <Wien. med. Wchnschr., v. 54 (26), 25. Juni, pp. 
1229-1232. [Wm.] 
1904 b. — [Fall von Amoebenenteritis.] [Demonstration & remarks, 9. Juni | 
<Mitt. d. Gesellsch. f. inn. Med. u. Kinderh. in Wien, v. 3 (10), pp. 
160-164. [Wm.] 
Vorwerk. [Dr.] 

1912. — Zur Pathologie und Hygiene von Garua (Deutsch-Adamaua) 
<Arch. f. Schiffs- u. Tropen-Hyg., Leipz., v. 16 (5), Marz, pp. 133-149, 
[Wa, Wm.] 
Waldow & Guehne. [Drs.] 

1912. — Erfahrungen mit Uzara bei Dysenterie. Vorlaufige Mitteilung 
<Arch. f. Schiffs- u. Tropen-Hyg., Leipz., v. 16 (6), Marz, p. 190. [Wa, 
Walker, Ernest Linwood. [Sc. D.] 

1908 a. — The parasitic amebae of the intestinal tract of man and other 
animals <J. Med. Research, Bost. (103), v. 17, n. s., v. 12 (4), Feb., pp. 
379-459, pis. 21 A, 22-24, figs. 1-16. [Wa, Wm.] 

1911. — A comparative study of the amoebae in the Manila water supply, 
in the intestinal tract of healthy persons, and in amoebic dysentery 
<Philippines J. Sc, Manila, B: Med. Sc, v. 6 (4), Oct., pp. 259-279, pis, 
1-5, figs. 1-16. [Wa.] 

Wallace, J. B. [M. D., Tampa, Fla.] 

1912. — Amoebic dysentery. [Read before Florida Med. Ass., Tampa, May 
8-10] <South. M. J., Nashville, v. 5 (10), Nov., pp. 688-692. [Wm.] 

Ward, Samuel B. [M. D.] . 

1903. — A case of dysentery due to double infection with the Uncinaria 
duodenalis and the Amoeba coli < Albany M. Ann., v. 24 (1), Jan., pp. 
23-26; note by Blumer, George, p. 26. [MS. dated June 2, 1902.] [Wm.] 
Wasdin, Eugene. [M. D., Charleston, S. C] 

1891 a. — Case of ameba dysentery; with autopsy <Med. News, Phila. (986), 
v. 59 (23), Dec. 5, pp. 656-657. [Wa, Wm.] 
von Wasielewski, Theodor Karl Wilhelm Nicholas. [Prof., Heidelberg.] 

1911. — Ueber Amobennachweis. [Read before Naturwissensch.-arztl. Ver. 
zu Heidelberg, 21. Nov. 1910] <Miinchen. med. Wchnschr., v. 58 (3). 
17. Jan., pp. 121-123, 1 fig. [Wa, Wm.] 

von Wasielewski, Theodor Karl Wilhelm Nicholas; & Hirschfeld [Dr.]. 

1909 a. — Zur Technik der Amobennntersuchimg <Hyg. Rundschau, Berl., 
v. 19 (16), 15. Aug., pp. 925-930. [Wa.] 


Watanabe, Yastaro. [Agric. College, Tohoku Imp. Univ.] 

1910. — On the so-called black-head of turkey. [Originally presented as 
Diss.] [English & Japanese text] <Tr. Sapporo Nat. Hist. Soc, Sapporo, 
Japan (1909-10), v. 3, pp. 67-81. [Wa.] 
Waugh, William Francis. [A. M., M. D. ; Prof., Therap., Bennett Med. College, 
Chicago, 111.] 
1908 a. — Dysentery : Recent observations on the treatment < Virginia M. 
Semi-Month., Richmond (296), v. 13 (8), July 24, pp. 181-183. [Wa, 
1910. — Amoebic dysentery < Toledo M. & S. Reporter, v. 36 (8), Aug., pp. 
359-361. [Wm.] 
Weichselbaum, Anton. [Prof., path. Anat., Wien.] 

1898 a.— Parasitologic <Handb. d. Hyg., Jena, v. 9 (2), pp. x+[63]-336, 
figs. 1-78. . [Wa, Wm.] 
Weidner, Carl. [Dr., Louisville, Ky.] 

1903.— [Discussion of Young, G. B., 1903, pp. 241-248] <Am. Pract. & News, 

Louisville, v. 35 (7-8), Apr. 1 & 15, pp. 291-292. [W T m.] 
1910.— [Discussion of Hanes, Granville S., 1910, pp. 1140-1146] < Kentucky 
M. J., Bowling Green, v. 8 (1), Jan. 1, p. 1148. [Wm.] 

1909.— [Discussion of Chantemesse & Rodriguez, 1909, pp. 29-32] <Bull. 
Soc. de path.-exot, Par., v. 2 (1), 13 Jan., pp. 32-33. [Wm.] 

Wellman, Frederick Creighton. [B. A., M. D., Tulane Univ., New Orleans, La.] 
1905 p. — Fatal case of blackwater fever supervening on amebic dysentery 

and showing malarial parasites in the blood <J. Am. M. Ass., Chicago, 

v. 45 (23), Dec. 2, p. 1736. [Wa, Wm, Wc] 
1907. — On an epidemic of enteric fever in the Angola highlands and on liver 

abscess in Angola <J. Trop. M. & Hyg., Lond., v. 10 (20), Oct. 15, pp. 

330-331. [Wa, Wm.] 

Wells, R. T. [M. A., M. B., Capt. I. M. S.] 

1911. — Aerial contamination as a fallacy in the study of amoebic infections 
by cultural methods. A preliminary note <Parasitology, Cambridge 
[Eng.], v. 4 (3), Oct. 24, pp. 204-219, pi. 6, figs. 1-28. [W T a.] 

W T enyon, C. M. [M. B., B. S., B. Sc. ; Protozool., Lond. School Trop. Med.] 

1907 i. — Observations on the Protozoa in the intestine of mice <Arch. f. 
Protistenk., Jena, Suppl. 1, Festbd. z. 25jahr. Prof.-Jubil. Richard 
Hertwig, pp. 169-201, 1 fig., pis. 10-12. [Wm.] 

1908 b. — Report of travelling pathologist and protozoologist <3. Rep. 
m Wellcome Research Lab., Khartoum, pp. 121-168, figs. 28-41, pi. 3, fig. 

[2] ; pis. 9-16. [Wa.] 
1908 k— Intestinal amoebiasis <Brit. M. J., Lond. (2495), v. 2, Oct. 24, pp. 

1244-1246. [Wa, Wm.] 
1912. — Experimental amoebic dysentery and liver-abscess in cats <J. Lon- 
don School Trop. M., v. 2 (1), Dec, pp. 27-34. [Wa.] 
Werner, Heinrich. [Stabsarzt, Schutztruppe f. Deutsch-Siidwestafrika.] 

1908 e. — Studien fiber pathogene Amoben <Beihefte z. Arch. f. Schiffs- u, 

Tropen-Hyg., Leipz. (11), Dec. 17, pp. 5-18 [pp. 423^36], pis. 1-6, figs. 

1-38. [Wm.] 
1909.— Studien fiber pathogene Amoben. [Abstract of remarks, 22. Sept. 

1908] <Verhandl. d. Gesellsch. deutsch. Naturf. u. Aerzte, Leipz. (80. 

Versaminl., Coin, 20.-26. Sept. 1908), 2. Teil, 2. Hillfte, med. Abt, p. 588. 



Werner, Heinrich — Continued. 

1909 b. — Studies regarding pathogenic amoebae. [Transl. of 1908 e, by 

W. .1). Sutherland] < Indian M. Gaz., Calcutta, v. 44 (7), July, pp. 241- 

245, 2 pis. [6 pis.], figs. 1-38. [Wm.] 
1911. — Entamoeba coli <Handb. d. path. Protozoen (v. Prowazek), Leipz., 

1. Lief., pp. 67-77, figs. 1-14, pi. 2, figs. 1-47. [Wa.] 
1912. — Ueber Uzara bei Amobendysenterie <Arch. f. Schiffs- u. Tropen-Hyg., 

Leipz., v. 16 (6), Miirz, pp. 190-192. [Wa, Wm.] 
Wesener, J. A. [Dr., Prof., Freiburg i. B.] 

1892 a. — L'nsere gegenwiirtigen Kenntnisse iiber Dysenterie in anatomischer 

und atiologischer Hinsicht <Centralbl. f. allg. Path. u. path. Anat., 

Jena, v. 3 (12), 1. Juli, pp. 484-496; (13), 26. Juli, pp. 529-545. [Wa, 

1892. — Le nostre odierne conoscenze sulla dissenteria. Dal punto di vista 

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496-506; (10), ott, pp. 544-555. [Wm.] 
West, H. A. [M. D. ; Prof., Theory & Pract. Med., Med. Dept, Univ. Texas; 

Sec'y, State Med. Ass. Texas.] 
1895. — Clinical notes on amoebic dysentery <Tr. 1. Pan. Am. M. Cong., 

Wash. (1893), pt. 1, pp. 301-306. [Wa, Wm.] 
W T esterveld, H. W. 

1908. — Een geval van chronische amoebendysenterie genezen door operatie 

<Nederl. Tijdschr. v. Geneesk., Amst, 52. Jaarg.. 2. R., 44. Jaarg., 2. 

Helft (15), 10 Oct., pp. 1224-1226. [Wa.] 
Weston, H. R. [First Lieut., Med. Reserve Corps, U. S. Army.] 

1912. — Balantidium coli as cause of dysentery in Philippine Islands <Mil. 

Surg., Wash., v. 30 (6), June, pp. 694-698. [Wm.] 
White, J. A. [M. D., U. S. Pub. Health & Mar.-Hosp. Serv., New Orleans, La.] 
1911. — The public health problems concerned in amebiasis. [Read at 8. 

Ann. Meet. Am. Soc. Trop. Med., New Orleans, May 18-19] <N. Orl. M. & 

S. J., v. 64 (2), Aug., pp. 111-116. [Wm.] 
Whitmore, Eugene R. [M. D., Manila, P. I.] 

1911. — Parasitare und freilebende Amoben aus Manila und Saigon und ihre 

Beziehungen zur Dysenterie <Arch. f. Protistenk., Jena, v. 23 (1-2), 

pp. 71-80, figs. 1-3. [Wa, W T m.] 
1911. — Studien iiber Kulturamoben aus Manila < Ibidem, pp. 81-95, pis. 

3-4, figs. 1-45. [Wa, Wm.] 
1911. — Vorliiufige Bemerkungen iiber Amoben aus Manila und Saigon <Cen- 

tralbl. f. Bakteriol. [etc.], Jena, 1. Abt, v. 58 (3), 1. Apr., Orig., pp. 

234-235. [Wa, Wm.] 
1912. — Parasitic amebas in the intestine of man, with a study of the Pro- 
tozoa found in the intestines of healthy men in the southern United 

States. Preliminary note <Arch. Int. Med., Chicago, v. 9 (4), Apr. 15, 

pp. 515-519. [Wm.] 
Whittington, J. B. [Dr., Resident Physician, Sheltering Arms Hosp., Hans- 
ford, W. Va.] 
1912. — Amoebiasis — report of case <W T est Virginia M. J., Wheeling, v. 6 

(10), Apr., pp. 343-344. [Wm.] 

1907.— [Discussion of Caussade & Joltrain, 1907, pp. 167-174] [15 fev.] 

<Bull. et mem. Soc. med. d. hop. de Par., 3. s., v. 24, pp. 177-178. [Wm.] 
Wijnhoff, J. A. 

1895.— Over Amoeburie <Nederl. Tijdschr. v. Geneesk.. Amst., 2. R., 31. 

Jaarg., Deel 1 (3), 19 Jan., pp. 107-117, 5 figs. [Wm.] 


Williams, Anna Wessels. [M. D.] 

1911. — Pure cultures of parasitic amebas on brain-streaked agar. [Abstract 
of paper read before 42. Meet. Cornell Univ. Med. Coll., N. Y., Feb. 15] 
<Proc. Soc. Exper. Biol. & Med., N. Y., v. 8 (3), pp. 56-58. [Wa.] 
1911. — Pure cultures of amoebae found in intestines of mammals < Collect. 
Studies Research Lab. Dept. Health N. Y., v. 6, pp. 298-308. [Wa, Lib. 
1911. — Pure cultures of amebae parasitic in mammals <J. Med. Research, 
Bost. (128), v. 25, n. s., v. 20 (2), Dec, pp. 263-283. [Wa, Win.] 
Williams, Anna Wessels; & Gurley, Caroline R. 

[1910]. — Studies on intestinal amebas and allied forms <Collect. Studies 
Research Lab. Dept. Health N. Y. (1908-09), v. 4, pp. 237-246. [Wa, 
Willis, D. O. [Dr., Leesville.] 

1912.— [Discussion of Simon, Sidney K., 1912, pp. 373-377] <N. Orl. M. & 
S. J., v. 65 (5), Nov., pp. 378-379. [Wm.] 
Wilson, Cunningham. 

1895 a. — Cases of amoebic dysentery <Jolms Hopkins Hosp. Bull., Bait. 
(54-55), v. 6, Sept.-Oct, pp. 142-143 % [Wa, Wm.] 
Wilson, Cunningham ; & Pressly, H. E. [M. D.'s, Birmingham, Ala.] 

1907. — Turnip top treatment of chronic diarrhea and amebic dysentery 
<J. Am. M. Ass., Chicago, v. 48 (10), Mar. 9, pp. 875-876. [Wa, Wm.] 
Witherspoon, E. O. [M. D. ; Prof., Dis. Rectum, Hosp. College Med., Louis- 
ville, Ky.] 
1906 a. — Amoebic infection of -the rectum <Med. Brief, St. Louis, v. 34 
(9), Sept., pp. 615-616. [Wm.] 
Witherspoon, J. A. [Dr., Nashville, Tenn.] 

1905.— [Discussion of Tuitle. James P., 1905, pp. 348-353] < Lancet-Clinic, 

Cincin., v. 94, n. s., v. 55, Sept. 23, p. 354. [Wm.] 
1909. — [Discussion of Bates, John Pelham, 1909, pp. 56-59] <J. Tennessee 
State M. Ass., Nashville, v. 2 (2), June, pp. 62-63. [Wm.] 
Withington, C. F. [M. D., Roxbury, Mass.] 

1894.— A case of amoebic dysentery. [Read before Boston Soc. Med. 
Improve., Mar. 12] <Boston M. & S. J., v. 130 (21), May 24, pp. 516- 
517. [W T m.] 
Wood, Horatio Curtis (jr.) ; & Fitz, Reginald H. 

1897 a. — The practice of medicine, x+1088 pp. 8°. Philadelphia. [Wm, 
Wood, J. William. [Dr.] 

1910. — [Four cases of amebic dysentery presented before Delaware Co. 
Med. Soc, Chester, Pa., Feb. 24] <Penn. M. J., Athens, v. 13 (7), Apr., 
pp. 573-574. [Wm.] 
Woodhull, Alfred A. [Brig. Gen., U. S. Army, retired.] 

1908 a. — Ipecacuanha in dysentery <Mil. Surg., Carlisle, Pa., v. 22 (2), 
Feb., pp. 114-115. [Wm.] 
Woodward, Joseph Janvier. [Surg., U. S. Army.] 

1879. — The medical and surgical history of the war of the rebellion. Part 
2, v. 2: Medical history. Being the second medical volume. Second 
issue, xii+869 pp., 42 figs., figs. A-B, 41 pis. fol. Washington. [Wm.] 
Woolloy, Paul Gerhnrrtt. [B. S., M. D. ; Prof., Path.; Dean, Med. Fac, Coll. 
Med., Univ. Cincinnati; Director, Lab. Cincinnati Hosp., Cincinnati, Ohio.] 
1905 ]>. Pathology of amebiasis. An acknowledgment. [Letter to editor, 
dated Oct.] <J. Am. M. Ass., Chicago, v. 45 (22), Nov. 25, p. 1671. 
[Wa, Wm, Wc] 


Woolley, Paul Gerhardt; & Musgrave, William E. 

1905 a. — The pathology of intestinal amoebiasifl < [Publication] (32), 

Bureau Govt. Lkb., Manila, June, pp. 31-48, pis. 1-23. [War.] 
1905 b. — The pathology of intestinal amebiasis. [Practically same as 

1905 a] <J. Am. M. Ass., Chicago, v. 45 (19), Nov. 4, pp. 1371-1378, 

figs. 1-27 (figs. 4-27 on 3 pis.) ; note by Woolley, Paul G. (22), Nov. 25, 

p. 1671. [Wa. Wm, Wc] 

Wuelker, Gerhard. [Dr.] 

1911. — Die Technik der Amobenziichtung <Centralbl. f. Bakteriol. [etc.], 
Jena, 1. Abt., v. 50 (19-21), 4. Dec., Ref., pp. 577-610. [Wa, Wm.] 


(1910 a).— [?] <Tr. N. York Acad. M., Jan. 7. 

1910 b. — Dysenterie amibienne traitee par l'appendicostomie. [Abstract of 
1910 a] <Presse med., Par., v. 18 (20), 9 mars, p. 173. [Wa, Wm.] 

Young, G. B. [M. D. ; Passed Asst. Surg., U. S. Pub. Health & Mar.-Hosp. 
3903. — Amoebic dysentery. [Read before Louisville Clin. Soc, Mar. 31] 
<Am. Pract. & News, Louisville, v. 35 (7-8), Apr. 1 & 15, pp. 241-248; 
discussion, pp. 288-294. [Wm.] 
Young, W. B. [M. D., Rock Hill, S. C] 

1910. — Amebae as the cause of pellagra <J. South Car. M. Ass., Charleston, 
v. 6 (11), Nov., pp. 585-589. [Wm.] 
Zacharias, Otto. [Dr., Ploen.] 

(1909). — Parasitische amoben in Volvox minor <Arch. Hydrobiol. Plank- 
tonkde., v. 5, pp. 69-70. 
Zancarol, George. [M. D. ; Surg., Greek Hosp.] 

1893 a. — Pathogenie des abces du foie <Rev. de chir., Par., v. 13 (8), 10 

aout, pp. 671-677. [Wm.] 
1895 a. — Dysenterie tropicale et abces du foie <Progres med., Par., an. 
23, 3. s., v. 1 (24), 15 juin, pp. 393-397. [Wm.] 

Zaubitzer, Hans. 

3901 a. — Studien fiber erne dem Strohinfus entnommene Amobe. Diss. 

45 pp., 1 1., 1 pi. 8° Marburg a. L. [Wm.] 
1901 b.— Idem <Arch. f. Hyg., Miinchen & Leipz.. v. 40 (2), pp. 103-142, 

pi. 1, figs. 1-74. [Wa, Wm.] 
Ziegler, Ernst. [Prof. Dr., Ordinarius f. allg. Path. u. path. Anat., Freiburg 

i. Br.; Editor, Beitr. z. path. Anat. u. z. allg. Path.] 
1883 a. — A text-book of general pathological anatomy and pathogenesis. 

Transl. and edited for English students by Donald Macalister. Pt. 1: 

General pathological anatomy, xv+371 pp., 117 figs. S°. New York. 


1883 b.— Idem, xvi+360 pp., 117 figs. 8°. London. [Wm.] 

1884 c. — Lehrbuch der aligemeinen und speciellen pathologischen Anatomie 
und Pathogenese. Mit einem Anhange liber die Technik der patho- 
logisch-anatomischen Untersuchung. Fur Aerzte und Studirende. 3. 
vermehrte u. verbesserte Aufl. 1. Theil : Allgemeine pathologische Ana- 
tomie. x+382 pp., 129 figs. 8°. Jena. [Wm.] 

1885 b. — Lehrbuch der aligemeinen und speciellen pathologischen Anatomie 
fiir Arzte und Studirende. 4. neu bearbeitete Aufl. v. 1 : Allgemeine 
pathologische Anatomie und Pathogenese. X+3S3 pp., 175 figs. 8°. 
Jena. [Wa.] 


Ziegler, Ernst — Continued. 

1S85 c. — A text-book of pathological anatomy and pathogenesis. Trans- 
lated and edited for English students by Donald MacAlister. Pt. 1: 
General pathological anatomy. 2. ed., xvi+360 pp., 117 figs. 8\ Lon- 
don. [Wa.] 

1887 c. — Lehrbuch der allgemeinen und speciellen pathologischen Anatomie 
fur Aerzte und Studirende. 5. neu bearbeitete Aufl. v. 1 : Allgemeine 
pathologische Anatomie und Pathogenese. xii+499 pp., 307 figs., 1 pi. 
8°. Jena. [Wm.] 

1887 d. — Idem. v. 2: Specielle pathologische Anatomie. x+1020 pp., 396 
figs. 8°. Jena. [Wm.] 

1889 a. — Idem. 6. verbesserte und theilweise neu bearbeitete Aufl. v. 1: 
Allgemeine pathologische Anatomie und Pathogenese. xiv+567 pp., 343 
figs., 1 pi. 4°. Jena. [Wa, Wm.] 

1890 a. — Idem. 6. neu bearbeitete Aufl. v. 2 : Specielle pathologische 
Anatomie. xii+1024 pp., 435 figs. 4°. Jena. [Wa, Wm.] 

1892 a. — Idem. 7. verbesserte und theilweise neu bearbeitete Aufl. v. 1 : 
Allgemeine pathologische Anatomie und Pathogenese. xi+638 pp., 386 
figs. 8°. Jena. [Wm.] 

1892 b. — Idem. v. 2 : Specielle pathologische Anatomie. x+1021 pp., 461 
figs. 8°. Jena. [Wm.] 

1892 c. — Traite d'anatomie pathologique generale et speciale. Trad, par 
la 6. ed. allemande (1889) et annote par G. Augier et E. van Ermengem. 
v. 1 : Anatomie pathologique generale et pathogenese. 751 pp., 329 figs. 
8°. Bruxelles. [Wm.] 

1895 a. — Lehrbuch der allgemeinen Pathologie und der pathologischen Ana- 
tomie. Fur Aerzte und Studirende. 8. neu bearbeitete Aufl. v. 1 : Allge- 
meine Pathologie. xii-f 746 pp., 458 figs. 8°. Jena. [Wm.] 

1895 b. — Idem. v. 2: Specielle pathologische Anatomie. xii+1025 pp., 562 
figs. 8°. Jena. [Wm.] 

1895 c. — General pathology, or the science of the causes, nature, and course 
of the pathological disturbances which occur in the living subject. Trans- 
lated from the 8. revised German edition. . . . Editor, Albert H Buck. 
xxii+588 pp., 458 figs., 1 pi. 8°. New York. [Wa, Wm, Wa] 

1897 a. — A text-book of special pathological anatomy. Translated and 
edited from the 8. German edition by Donald MacAlister and Henry W. 
Cattell. Sect, ix-xv. xv +579-1221 +i-xxxi pp., figs. 309-562. 8°. New 
York. [Wa] 

1898 a. — Lehrbuch der allgemeinen Pathologie und der pathologischen Ana- 
tomie. Fur Aerzte und Studirende. 10. neu bearbeitete Aufl. v. 1 : Allge- 
meine Pathologie. xii+747 pp., 544 figs. 8°. Jena. [Wm.] 

1898 b. — Idem. v. 2 : Specielle pathologische Anatomie. xii+1024 pp., 656 
figs. 8°. Jena. [Wm.] 

1899 a. — General pathology [etc.]. Transl. from 9. revised German ed. . . . 
xii+598 pp., 544 figs. 8°. New York. [Wm, Wc] 

1901a. — Lehrbuch der allgemeinen Pathologie und der pathologischen Ana- 
tomie. Fur Aerzte und Studirende. 10. neu bearbeitete Aufl. v. 1 : Allge- 
meine Pathologie. xii+798 pp., 586 figs. 8°. Jena. [Wm.] 

1902 a. — Idem. v. 2: Specielle pathologische Anatomie. xiv pp., 1 1., 999 
pp., 723 figs. 8°. Jena. [Wm.] 

1908 a: — General p.ithology, or the science of the causes, nature, and course 
of the processes of disease. Translated from the 10. revised German edi- 
tion, and edited by Aldred Scott Warthin. xxiii+760 pp., 586 figs. 8°. 
Now York. [Wa, Wm, Wc] 


Ziegler, Ernst — Continued. 

1905. — Lehrbuch der allgemeine Pathologie und der pathologischen Ana- 
tomie fiir Aerzte und Studierende. 11. neu bearbeitete Aufl. v. 1: Allge- 
meine Pathologie. x+810 pp., 604 figs. 8°. Jena. [Wm.] 

1906. — Idem. v. 2: Specielle pathologische Anatomie. xi+1098 pp., 798 
figs. 8°. Jena. [Wm.] 

1908 a. — General pathology. Transl. from the 11. revised German edition. 
Edited and brought up to date by Aldred Scott Warthin. xx+781 pp., 604 
figs. 8°. New York. [Wa, Wc] 
Zorn, Ludwig. 

1901a. — Beitrag zur Kenntnis der Amoebenenteritis. Diss. 32 pp. 8°. 
Miinchen. [Wm.] 

1902 a.— Idem <Deutsches Arch. f. klin. Med., Leipz., v. 72 (3^), 16. Mai, 
pp. 366-379. [Wm.] 
Zusija, I. 

1893 a. — Ueber die Amoeben im Darminhalt der Ruhrkranken. [Japanese 
text] <Ztschr. d. med. Gesellsch. zu Tokyo, v. 7 (22), 20. Nov., pp. 19-22. 
[W r m.] 
Zusija, I. ; & Naniwa, K. 

1893 a. — Ueber die Amoeben im Darminhalt der gesunden Menschen. [Japa- 
nese text] <Ztschr. d. med. Gesellsch. zu Tokyo, v. 7 (22), 20. Nov., pp. 
16-19. [Wm.] 


africana (Hartinann, 1907) Brumpt, 1910, 32.— Dopter, 1910, 126. 

blattae Buetschli, 1S78 a, 273-277, pi. 15, fig. 26 a-d.— Braun, 1895 b, 43.— 
Braun & Luehe, 1909, 2, 20; 1910, 3, 21 (blattoea).— Chatton, 1910, 249; 
1912, 111.— Chatton & Brodsky, 1909, 9.— Doflein, 1901 a, 19-20, fig. 8; 
1907, 281 ; 1909, 99, fig. 106 ; 1911, 107, fig. 120.— Elmassian, 1909, 143-163, 
figs, a-g, pi. 11, figs. 1-33; 1909, 340, 344.— Gerould, 1906, 707-710.— 
Grassi, 1882 a, 184.— Grosse-Allemann, 1909, 213.— Gruber, 1911, 256.— 
von Janicki, 1908, 148-151.— Leidy, 1879 a, 300; 1879 k, 204-205: 1904 a, 
156-157 ; 1905 a, 156-157.— Mercier, 1907, 1132^1134 ; 1908, 942-945 ; 1909, 
164-168; 1910. 144.— Metcalf, 1910, 309, 316.— Minchin, 1907, 17, 20; 1909, 
17; 1910, 300.— Pfeiffer, 1890 c, 801.— Porter. 1909, 40.— Rhumbler, 1898, 
111, 119, 124, 147, 151, 152, 156, 166, 170, 191, figs. 4, 18, 23, 35, 37; 1905 
Cj 3_4, 7_8, 10-13, 31, 39, 40, figs. 1, 5, 7, 8, 9, 19, 22.— Schepotieff, 1910, 
495, 496, 497, -199, 503, 505.— Schneidemuehl, 1896 a, 259.— Schneider, 
K. C, 1905 a, 24, 28, 29, 91, 111, pi. 2, fig. 6 (blattarum).— Schubotz, 
1905 a, 1^2, pi. 1, figs. 1-10, pi. 2, figs. 1-6; 1905 b, 1-42, pi. 1. figs. 1-10, 
pi. 2, figs. 1-6.— Stiles, 1905 e, 294. 

blattarum Cnlandruccio, 1890 a, 99.— Casagrandi & Barbagallo, 1897, 113, 
152, 163; 1897 a, 586, 589.— Doflein, 1909, 18, fig. 7; 1911, 18, fig. 7.— 
Grassi, 1888 b, 12.— Pfeiffer, 1S91 a, 211, fig. 88 a.— Stiles, 1905 e, 294.— 
Vahlkampf, 1905 a, 203.— Wuelker, 1911, 609. 

blochmanni Doflein, 1901 a, 17-18, figs. 5-7.— Chatton, 1909, 690; 1910. 
248.— Doflein, 1909, 514, fig. 455; Doflein, 1911, 584, fig. 517. 

bovis Doflein, 1909, 499; 1911, 598.— Gedoelst, 1911, 32.— Liebetanz, 1905 a, 
314; 1910, 40^1.— Walker, 1908 a, 424, 441. 

buccalis Steinberg, 1862 a. — Artault, 1898, 276.— de Beaurepaire Aragfio. 

1909, 36.— Blanchard, 18S5 g, 16; 1896 b, 657.— de Bonis, 1882 a, 146.— 
Braun, 1883 a, 11; 1895 b, 44; 1903, 38; 1906, 37; 190S, 42.— Brumpt. 

1910, 31.— Craig, 1911, 230.— Doflein, 1901 a, 31; 1909, 147; 1911, 158.— 


Amoeba — Continued . 

buccalis — Continued. 
Doflein & von Prowazek, 1903, 927— Dunglison, 1893 a, 48.— Futcher, 
1903 d, 481.— Gedoelst, 1911, 32.— Guiart, 1910, 137.— Hickson, 1909, 84.— 
Ijima, 1889 b, 57.— Kartulis, 1893 a, 12; 1906, 354.— Leuckart, 1876 a, 
844 ; 1S86 d, 187, 241.— Mincbin, 1907, 17, 18, 21 ; 1909, 17-18, 21.— Moniez, 
1896 a, 17.— Pfeiffer, L„ 18SS c, 666.— Railliet, 1885 a, 150; 1893 a, 118.— 
Ruge, 1906 b, 9.— Scbneideinuebl, 1896 a, 259.— Spalikowski, 1897 a, 
1056.— Stengel, 1892 a', 287.— Stiles, 1905 e, 296.— Tanaka, 1903, 5.— 
Verdun, 1907 a, 41.— Walker, 1908 a, 423, 442. 

chaetognathi Grassi, 1882 a, 1S5-1S7, pi. 4, figs. 3, 4, 5, 6, 17, 27.— Doflein, 
1901 a, 20.— Pfeiffer, L,, 1S88 c, 665; 1S90 e, 801; 1891 a, 212 (cbaetog- 
nati).— Porter, 1909, 40. 

chironomi Porter, 1909, 32-41, figs. 1-21.— Alexeieff, 1912, 68, 70.— Greig & 
Wells, 1911, 14. 

ciliaria Grabani, 1899 a, 477^82 (ciliata, 515-520). 

cobayae Walker, 1908 a, 429, 442, pi. 22, figs. 1-3, pi. 23, fig. 10 (copayae, 
429).— Gedoelst, 1911, 33.— Williams, 1911, 268, 271.— Williams & Gurley, 
1910, 245 (cobaye). 

coli Loescb, 1S75 a, 196-211, pi. 10, figs. 1-3.— Abbott, 1899, 97.— Albu, 1905, 
432, 434, 435.— Anderson, 190S, 1243.— Axisa, 1910, 667-699.— Baelz, 1883 
a, 237.— Barbagallo, 1905, 73, 74, 75; 1905, 145, 146; 1906, 380-381.— 
Bassett-Smitb, 1900 a, 33-34.— Beijerinck, 1896 a, 261.— Bertarelli, 1905, 
193-198; 1905, 397-399.— Bizzozero, 1882 a, 136; 1883, 134; 1887, 191- 
192.— Blancbard, 1885 g, 10-14, 15, fig. 6.— Blumer, 1903, 26.— Boas, 1911, 
121.— de Bonis, 1882, 146.— Bootb, 1908, 340, 341, 342.— Borini, 1904, 12- 
16, fig. 1.— Bose, 1908, 1250.— Bosso, 1895 a, 651.— Brannan, 1893, 317- 
319.— Brau, 1908, 512.— Braun, 1883 a, 10-11 fig. 1 ; 1895 b, 34-44, figs. 1, 
2, 3, 4 ; 1903, 32, figs. 1, 3, 4 ; 1906, 30, 31, fig. 1 ; 1908, 36— Broido, 1903, 
821, 824, 827.— Brumpt, 1909, 20; 1910, 20.— Buchanan, R. E., 1911, 416 ; 
418.— Buchanan, W. J., 1900, 306.— Cahen, 1891 a, 854.— Calandruccio, 
1890 a, 95, 99-100.— Calkins, 1901 b, 63.— Casagrandi & Barbagallo, 1896 
c, 471 ; 1897 a, 579, 580, 584, 585, 586, 587, 588, 589 ; 1897, 103-166, pi. 2, 
figs. 1-26.— Castellani, 1904, 497, 498, 499, 500, 507, 509; 1905, 68.— Cayley, 
1893, 630.— Celli, 1896 b, 538.— Celli & Fiocca, 1S94 b, 435, 437, 441 ; 1894 
e, 330, 333; 1895 d, 309, 310.— Chatton & Lalung-Bonnaire, 1912, 142.— 
Chlapowski, 1909. 86.— Ciechanowski & Nowak, 1897, 855.— Cooke, 1910, 
1148 ; 1910, 598 ; 1910; 325-331.— Councilman, 1892 c, 1-7.— Councilman & 
Lafleur, 1891 a, 397, 405 [5, 13].— Craig, 1901 a, 414-418; 1904, 146, 154; 
1904, 185, 186 ; 1904, 299-301, figs. 1-8 ; 1905, 243, 244 ; 1908, 327, 329, 330, 
331 ; 1911, 2, 30, 31, 33, 34, 35 ; 1912, 31 ; 1912, 2.— Cramer, 1896 a, 139, 
140, 141, 142, 143.— Crowell, 1910, 77.— Cunningham, 1881 a, 236, 285, 
286.— Daland, 1892, 806 (colli).— Daniels, 1902 b, 45.— Daniels & Stanton, 
1907. 352, 354.— Darnall, 1901, 229-232.— Davidson, 1893, 549, 583.— 
Deeks & Shaw, 1911, 2.— Delafield & Prudden, 1897 a, 127, 128, 130, fig. 
30; 1901, 128, 511, figs. 51, 294.— Denier & Huet, 1912, 263.— Diamond, 
1900 a, 817-820. 1 fig.— Dievitski, 1903, 774-785.— Dock, 1902 a, 617-619.— 
Doflein, 1901 a, 20-27, 31, figs. 9-14.— Doflein & von Prowazek, 1903, 883, 
884, 892, 911. 913-920, fig. 32.— Dopter, 1910, 125, 126. 200.— Duncan, 1902, 
841.— Dunglison, 1893 a, 48, 1185 (Appendix, 1895 a).— Ebstein, 1901 a, 
449.— Eiehberg, 1891 a, 201-205.— Eichhorst, 1901 a, 292, fig. 28.— Fajardo, 
1896 a, 754, 755, 765.— Fenoglio, 1890, 62-70; 1900, 415-419; 1904, 245- 
267.— Fernando, 1904, 56.— Finley & Adami, 1895, 375-378.— Flexner, 
1900, 1202; 1900 a, 930; 1900 c, 918; 1901, 297-337; 1907, 532, 533; 1909, 


Amoeba — Continued. 
coli — Continued. 

532, 533.— Funkhouser, 1903, 343.— Futcher, 1903 d, 480, 481.— Gabbi, 

1906, 450.— Galloway, 1894, 676-677.— Gasser, 1895 a, 199.— Gauducheau, 

1907, 487.— Gedoelst, 1911, 31, fig. 30.— Gerry & Fitz, 1891 a. 5*2 .",!»:>,.— 
Goltman, 1903, 75.— Gould, 1891, 107-108.— Gradwohl, 1903, 344.— Grass!, 
1879 n, 445, 446; 1882 a, 178-181, 200-207, 218, 219, pi. 3, fig. 45; 1888 1» 
6, 12; 1888 e, 83, 84.— Gross, 1903, 432.— Grosse-Allermann, 1909, 252.— 
Guiart, 1910, 140, 141, 142, 143, 257.— de Haan & Kiewiet de Jonge, 1908, 
316.— Harold, 1892 a, 1429.— Harris, 1892 a, 631; 1901, 191-194; 1901, 
69.— Hart, 1903 a, 380.— Hartmann, 1908, 117 [217]; 1909, 208; 1911, 
50.— Head & Ulrich, 1904, 249-250.— Hehir, 1892 b, 321-323.— Holt, 1907, 
920-923 ; 1907, 517, 518, 521 ; 1908, 2140-2143 ; 1909, 39^19.— Hoppe-Seyler, 
1901, 149, 150, 151 ; 1904 a, 647.— Howard, 1892 a, 705-710.— Hoyt, 1908, 
26; 1908, 417.— Huber, 1909, 265.— Huber, J. Ch., 1906, 1609.— Ijima, 
1889 b, 54.— Jaeger, 1901a, 91S, 919; 1902 c, 209, 210; 1902 e. 865-8G7 ; 
1902 g, 556.— von Jakscb, 1888 a, 512; 1896 a, 251-252, fig. 73 c— Janow- 
ski, 1897 c, 92, 96, 97, 154, 156, 157, 194, 195, 197, 198, 199, 200, 234, 
239, 240, 241, 242, 243, 244, 246. 250, 251.— Jeffries, 1904 a, 356.— Jensen, 
1898 a, 133, 138, 139.— Johnson, 1908, 377-378.— Juergens, 1907, 771, 777.— 
Kaestner, 1906, 10-12, figs. 1-3.— Kartulis, 1885 c, 145; 1886 a, 524; 
1887 b, 745; 1889 a, 97; 1890 b, 54; 1891 a, 365.— Kiewiet de Jonge, 
1904 a, 74, 77.— Killougb, 1908, 371-377 ; 1909, 174-176.— Kovacs, 1892 a, 
509-551.— Kruse & Pasquale, 1893 a, 354. 378; 1894 a, 113.— Kruse, 
W. A. K., 1896 a, 606-618.— Kuenen, 1909, 547, 630, 632, 633.— Kurtz, 
1903, 535-542.— Lafleur, 1890 a, 91-92 ; 1891 a, 83-84 ; 1895, 379 ; 1897 a, 
753-783.— Lamb, 1907, 354-356.— Laveran, 1893 h, 876, 877.— Lehmann, 
1912, 591.— Lemoine, 1908, 640-643.— Leuckart, 1879 b, 236; 1886 d, 186- 
191, fig. 94.— Lindner, 1896 a, 1231.— Liston, 1911, 108.— MacCallum, 1906, 
28, 29, 30.— McElroy, 1902, 169-176.— McMillan, 1912, 48.— Maggiora, 1891, 
718, 719, 723, 724, 725, 726 ; 1892 a, 173, 174, 176, 177, 178, 179, 183, 184.— 
Manson, 1894, 676-678, 1 fig. ; 1901 b, 266 ; 1904. 379, 384, 390, 393, 394, 
395, 456, 458, 459, fig. 55 ; 1907, 434, 437, 443, 444, 446, 466, 498. fig. 61.— 
Martin, C. F., 1911, 643.— Martin, F. S.. 1905 a, 379.— Martini, 1910, 390 ; 
1911, 395.— Messineo, 1911, 241, 242, 243.— Miller, 1894 a, 275.— Minchin, 
1907, 17, 18, fig. 1; 1909, 17, 18, 20, fig. 1.— Molisch, 1903, 22.— Moniez, 
1896 a, 2, 3-12, 14, 15, 16, 18, 69, figs. 1, 2.— Mosler & Peiper, 1894 a, 1-6, 
fig. 1.— Motas, 1906, 682.— Moulden, 1906 a, 132-135.— Musgrave, 1906 a, 
554.— Musgrave & Clegg, 1904 h, 5-85 ; 1908 m, 343, 346 ; 1906, 922, 946.— 
Musser, 1900 b, 1263.— Myer, 1902 a, 19.— Neveu-Lemaire, 1902 a, 6, 8, 9. 
1 fig. ; 1904 a, 6, 9, 1 fig.— Newell, H. A., 1910, 100.— Nietert, 1902, 55-01.— 
Niles, 1908, 420-424.— Normand, 1879 a, 211.— Opie, 1901, 219.— Oppen- 
beim, 1900 a, 164-165.— Osier, 1890 b, 53-54 ; 1890 d, 736 ; 1895, 144 ; 1898 a, 
195, 201, 577; 1902 c, 673-677.— Patterson, 1909, 198-202.— Perroncito, 
1882 a, 85; 1912, 29-30.— Peyrot & Roger, 1897, 89.— Pfeiffer, L., 1SS8 c, 
662, 663, 664, 665 ; 1891 a, 210-215, fig. 88 d.— Phoustanos, 1906, 65-69, 97- 
104.— Piccardi, 1895 a, 171, 174, 180, 181.— Posner, 1893 c, 674, 676.— Prues, 
1905, 7-109.— Quincke, 1899 a, 1002, 1032, figs. 2, 3.— Quincke & Roos, 
1893 a, 1093, 1094.— Railliet, 1885 a, 150; 1893 a, 116-117, fig. 54.— Rhein, 
1892 a, 40-41.— Rho, 1894 a, 16.— Roger, 1901a, 115, 118.— Roos, 1S94 c, 
3S9, 390, 393, 399, 400 404.— Rose, 1910, 36.— Rosenberger, 1912, 590-591.— 
Ruge, 1906 b, 11.— Satterthwaite, 1881 b, 219, 1 fig.— Schaeffer. 1901 a, 
404; 1901 b, 657.— Schardinger, 1896 a, 544-545; 1899 a, 722, 723, 724.— 
Schaudinn, 1903 a, 547, 550, 564.— Schneidemuehl. 1896 a, 258-259.— 


Amoeba — Continued. 

eoli — Continued. 

Schuberg, 1893 a, 59S, 654, 701.— Schubotz, 1905 b, 5.— Scott, J. A., 1901, 
11-15.— Seifert, 1908 a, 481, 485.— Shaw, 1901, 601, 620; 1905, 642, 663; 
1909, 655, 680.— Shiga. 1898, 819, 821; 1902 a, 352, 353.— de Silvestri, 
1895, 33.— Simon, C. E., 1890 a, 97; 1896 a, 183, 214, 225, 469; 1897 a, 
210, 241, 259, fig. 42; 1904 a, 299^300, 353, 629, fig. 56; 1907, 286, 339; 
1911, 215, 262.— Simon, S. K., 1909, 1528.— Slaughter, 1895 a, 722-731.— 
Smith, A. J., 1901, 409-412.— Smith, A. J.. & Weidman, 1910, 286.— 
Smith, R. J., 1906, 420-422.— Sonsino, 1896 a, 309.— Spelman & Wherry, 
1906 a, 277-279.— Steffenhagen, 1903 a, 22, 23.— Stengel, 1890 a, 500-503, 
figs. 1-3; 1891, 99-101; 1891 b, 218-224; 1892 a, 286-293; 1898, 103- 
110.— Stiles, 1902 hh, 211 ; 1905 e, 292-303 ; 1907 e, 532.— Stockton, 1894, 
69-73.— Streett, 1893, 92-99.— Strong, L. W., 1898 a, 249-259.— Strong, 
R. P., 1901 c, 10-11; 1901, 742-743; 1907 a, 494.— Talamon, 1891 b, 550- 
552.— Tanaka, 1903, 1-29.— Tayler-Jones, 1904, 13.— Taylor, 1903 a, 10.— 
Thayer, W. S., & Flexner, 1893 a. 56-58.— Tuttle, 1904 a, 561.— Vahl- 
kampf, 1905 a, 198, 199, 201, 202, 203, 206.— Vedder, 1906 a, 870; 1907 a, 
192.— Verdun, 1904 d, 183-185; 1904 1 386, 387, 388, 389, 390, 391, 392, 
394; 1907 a, 21, 28, 29, 30-32, 33, 34, 36, 37, 43-44, figs. 1, 2, 3, 4, pi. 1, 
fig. 1.— Viereck, 1906 e, 1063; 1907 c, 28, 32, 33.— Vivaldi, 1894 a, 148.— 
Vollbracht, 1904 b, 161.— Walker, 1908 a, 382, 386, 387, 389, 392, 393, 411, 
412, 413, 418. 419, 420, 422, 424, 428. 429, 430, 431, 432, 440, 442, pi. 22, fig. 
4, pi. 23, fig. 7.— Ward, 1903 a, 23-26.— Weichselbaum, 1898 a, 282-283, fig. 
54.— Wellman, 1905 p, 1736.— Wenyon, 1907 i, 182.— Werner, 1911, 67.— 
Wesener, 1892 a, 541 ; 1892, 548, 550.— West, 1895, 301-306.— Wijnhoff, 1895, 
107.— Williams. 1911, 267, 271, 273, 275, 276, 277, .279, 280.— Williams & Gur- 
ley, 1910, 239, 245.— Withington, 1894, 516-517.— Wood, H. C, & Fitz, 1897 a, 
321.— Woodward, 1879, 371.— Woolley & Musgrave, 1905 a, 31-48 ; 1905 b, 
1371-1378.— Wuelker, 1911, 609.— Zaubitzer, 1901 b, 138.— Ziegler, 1883 a, 
353 ; 1883 b, 345 ; 1884 c, 373 ; 1885 b, 373 ; 1885 c, 345 ; 1887 c, 48S ; 1887 d, 
554 ; 1889 a, 551 ; 1892 a, 616 ; 1892 c, 727 ; 1895 c, 564 ; 1898 a, 716 ; 1899 a, 
571 ; 1903 a, 680 ; 1908 a, 689.— Zom, 1901 a, 8, 11, 28, 29 ; 1902 a, 371, 372, 

eoli communis Kruse, W. A. K., 1896 a, 613. — Fenoglio, 1904, 247. — Mes- 
sineo, 1911, 241. 

eoli var. dysenteriae Doflein & von Prowazek, 1903, 918. — Jensen, 1898 a, 
134 (eoli dysenterica ) . — Messineo, 1911, 241. 

eoli dysenterici Kruse, W. A. IC, 1896 a, 613.— Fenoglio, 1904, 247. 

eoli felis Quincke & Roos, 1893 a, 1093, 1094.— Barbagallo, 1905, 73; 1905, 
283.— Borini, 1904, 14.— Braun, 1895 b, 41. — Casagrandi & Barbagallo, 
1897, 110, 133, 136, 148, 150.— Chlapowski, 1909, 86.— Ciechanowski fr 
Nowak, 1897, 855.— Craig, 1905, 854.— Cramer, 1896 a, 141.— Dock, 1902 a, 
619.— Eichhorst, 1901 a, 292.— Fajardo, 1896 a, 755.— Funkhouser, 1903, 
343.— Futcher, 1903 d, 481.— Hoppe-Seyler, 1901, 149, 151, fig. 10; 1904 a, 
647.— Jaeger, 1902 c, 210.— Janowski, 1897 c, 234.— Moniez, 1896 a, 6.— 
PruSs, 1905, 39.— Quincke, 1899 a, 1002, 1032, 1034.— Schaudinn, 1903 a, 
564.— Schneidemuehl, 1896 a, 259.— Shiga, 1898, 819.— Steffenhagen, 1903 
a, 22, 23.— Stiles, 1905 e, 295.— Tanaka, 1903, 16.— Verdun, 1904 f, 391; 
1905 a, 58; 1907 a, 30, 37.— Vollbracht, 1904 b, 163.— Walker, 1908 a, 422, 
430, 440, 442-443.— Ziegler, 1908 a, 690, fig. 524.— Zorn, 1901 a, 11, 12; 
1«)02 a, 371 , 378. 

toll hominis Kuenen, 1909, 564. 


Amoeba — Continued . 

coli incapsulata Maggiora, 1891, 725; 1892, 178. — Mosler & Peiper, 1894 a, 
3.— Steffenhagen, 1903 a, 4. 

coli intcstini vulgaris Fenoglio, 1904, 252. 

coli 'mitis Quincke & Roos, 1893 a, 1093, 1094.— Barbagallo, 1905, 73 ; 1905, 
283.— Borchardt, 1896 a, 87.— Borini, 1904, 14.— Braun, 1895 b, 41; 1903 
37, 38; 1908, 35— Broido, 1903, 824.— Casagrandi & Barbagallo, 1897, 110, 
133, 134, 136, 148, 150.— Chlapowski, 1909, 86.— Omncilman & Lafleur. 
1891 a, 440.— Craig, 1905, 243; 1905, 854; 1908, 329; 1911, 30.— Cramer, 
1896 a, 141.— Dock, 1902 a, 619.— Doflein & von Prowazek, 1903, 911 — 
Ebstein, 1901 a, 448.— Eichhorst, 1901 a, 292.— Fajardo, 1896 a, 755 — 
Fenoglio, 1904, 247, 252.— Flexner, 1901, 309; 1907, 532; 1909, 532.— 
Funkhouser, 1903, 343.— Fu tcher, 1903 d, 481.— Hoppe-Seyler, 1901, 149, 
150, 160, 166, fig. 9.— Jaeger, 1902 c, 210.— Janowski, 1897 c, 194, 197, 202, 
234.— Jensen, 1898 a, 134.— Kruse, W. A. K., 1896 a, 613.— Messineo, 1911, 
241.— Meyer, 1906, 1327.— Moniez, 1896 a, 6.— PruSs, 1905, 38, 39.— 
Quincke, 1899 a, 1002, 1003, 1032, 1034.— Roos, 1894 c, 390, 391, 397, 399, 
405.— Ruge, 1906 b, 3, 11.— Schaudinn, 1903 a, 564.— Schneideinuehl, 1896 
a, 259.— Shiga, 1S98, 819.— Steffenhagen, 3903 a, 22, 23.— Stengel, 1898, 
109.— Stiles, 1905 e, 295.— Strong, L. W., 1898 a, 255.— Talamon, 1891 b, 
550-552.— Tana ka, 1903, 16.— Verdun, 1904 f, 391, 392; 1905 a, 58; 1907 a, 
37.— Vincent, 1903 a, 880.— Walker, 1908 a, 422, 430, 440, 443.— Weichsel- 
baum, 1898 a, 283.— Ziegler, 1895 a, 717, fig. 444; 1895 c, 563, fig. 444; 
1898 a, 715, 716, fig. 530 ; 1899 a, 570, 571, fig. 530 ; 1901 a, 719, fig. 513 : 
1903 a, 680, fig. 513; 1905, 723, fig. 523; 1908 a, 689.— Zorn, 1901 a, 11, 
12; 1902 a, 371. 

coli vulgaris Ziegler, 1895 a, 717 ; 1895 c, 563 ; 1898 a, 715, 716 ; 1899 a, 570 ; 
1901 a, 719; 1903 a, 680; 1905, 723; 1908 a, 689.— Broido, 1903, 829.— 
Casagrandi & Barbagallo, 1897, 150.— Ciechanowski & Nowak, 1897, 855 — 
Strong, L. W., 1898 a, 255. 

croupogena Rivolta & Delprato, 1881 a. — Perroncito, 1882 a, 95 (crupo- 
gena).— Railliet, 1893 a, 148. 

currens Metcalf, 1910, 308-310, fig. 24. 

dentalis Braun, 1883 a, 11; 1895 b, 44; 1903, 38; 1906, 37; 1908, 42.— 
Brumpt, 1910, 32.— Craig, 1911, 37.— Doflein, 1911, 595.— Doflein & von 
Prowazek, 1903, 927.— Dunglison, 1893 a, 48.— Guiart, 1910, 137.— Kruse, 
W. A. K., 1896 a, 617.— Leuckart, 1886 d, 187.— Moniez, 1896 a, 16 — 
Railliet, 1893 a, 118.— Schneidemuehl, 1896 a, 259.— Stiles, 1905 e, 296.— 
Tanaka, 1903, 5.— Verdun, 1907 a, 41.— Walker, 1908 a, 423, 443. 

diaphana Celli & Fiocca, 1894 b, 435, 438, 440; 1894 e, 330, 331, 334-335, 
338.— Blanchard, 1896 b, 656.— Booth, 1908, 341.— Borini, 1904, 15 — 
Braun, 1903, 38; 1908, 35— Casagrandi & Barbagallo, 1897, 140, 147, 
151._Celli, 1896 b, 538.— Celli & Fiocca, 1895 d, 310.— Craig, 1908, 329; 
1911, 32.— Cramer, 1896 a, 142.— Doflein & von Prowazek, 1903, 912.— 
Gedoelst, 1911, 31.— Janowski, 1897 c, 239, 240, 241, 242.— Manson, 1904, 
394; 1907, 444.— Moniez, 1896 a, 12, 13, 14.— Phoustanos, 1906, 68.— 
Pru§s, 1905, 27.— Stiles, 1905 e, 295.— Strong, R. P., 1907 a, 495.— Vahl- 
kampf, 1905 a, 202.— Verdun, 1907 a, 29.— Walker, 1908 a, 430, 431, 443. 

dysenteriac Councilman & Lafleur, 1S91 a, 405 (13).— Abbott, 1899, 97.— 
Albu, 1905, 436.— Blanchard, 1896 b, 658.— Braun, 1895 b, 42; 1903, 37; 
1908, 35.— Broido, 1903, 822, 824.— Brumpt, 1910, 20.— Brunwin, 1908, 
278.— Buchanan, R. E., 1911, 419.— Charles, 1908, 123S.— Ciechanowski & 

66692— vol 2, pt 1—13 18 


Amoeba — Continued. 

dyscnteriae — Continued. 

Nowak, 1897, 855.— Craig, 1905, 243, 244, 245 ; 1908, 328, 329, 330 ; 1911, 6, 
31, 33, 35.— Cramer, 1896 a, 139, 140, 141, 143, 144.— Culler, 1910, 500-501.— 
Deeks & Shaw, 1911, 2, 3.— Delafield & Prudden. 1897 a, 127.— Denier & 
Huet, 1912, 263, 264, 265.— Dock, 1902 a, 619.— Doflein & von Prowazek, 
1903, 918.— Dopter, 1905, 365 ; 1905, 417 ; 1907, 505-541 ; 1910, 117, 124. — 
Dunglison, 1893 a (Appendix, 1895 a, 1185).— Flexner, 1892 c, 104, 106; 
1901, 309 ; 1907, 532 ; 1909, 532.— Funkhouser, 1903, 343.— Futcher, 1903 d, 
480-488.— Gant, 1906, 259, 260.— Gedoelst, 1911, 31, fig. 31.— Goodhue, 
1906, 1583.— Gross, 1903, 432.— Guiart, 1910, 141, 143, 150, 257.— Herriek, 
1910, 663.— Holt, 1907, 520.— Hoppe-Seyler, 1901, 150, 151 ; 1904 a, 647.— 
Jaeger, 1901 a, 918; 1902 c, 209, 210; 1902 g, 556.— Janowski, 1S97 c, 
154, 195, 198.— Jelks, 1902, 632.— Killough, 1908, 372 ; 1909, 174.— Kruse & 
Pasquale, 1894 a, 113.— Laflenr, 1897 .a, 761.— Lockwood, 1897 b, 475.— 
Macfadyen, 1893, 114.— McMillan, 1912, 48.— Manson, 1901 a. 262; 1904, 
391, 393; 1907, 443.— Marshall, D. G., 1899 a, 1386-1388, figs. 1-5.— 
Martin, 1905 a, 378, 379.— Matthews, 1905, 253.— Musgrave & Clegg, 
1905 in, 346.— Neveu-Lemaire, 1912, 197.— Osier, 1898 a, 195.— Pat- 
terson, 1908, 189, 190; 1910, 835 (dysenterii).— Piccardi, 1895 a, 182.— 
Rogers, 1908, 285-290.— Rcos, 1894 c, 393, 399, 404.— Ruge, 1906 b, 
3, 5.— Rutherford, 1903 a, 73-77.— Shaw, 1901, 620, fig. 221; 1905, 663, 
fig. 262; 1909, 680, fig. 262.— Shiga, 189S, 818; 1902 a, 352, 353.— Simon, 
S. K., 1909, 1528.— Steffenhagen, 1903 a, 23.— Stiles, 1905 e, 295, 297; 
1907 e, 532.— Strong, L. W., 1898 a, 255.— Strong, R. P., 1901 c, 7-10 ; 1901, 
741-742, 743; 1907 a, 494.— Tanaka, 1910, 2300-2301.— Taylor, 1903 a, 10 
(dysenteria).— Thomas, 1906 a, 108-118.— Tuttle, 1904 a, 1022-1026; 
1904 b, 561-571; 1905, 348-353.— Verdun, 1904 f, 3S9 ; 1905 a, 58; 1907 a, 
30.— Viereck, 1906 e, 1063; 1907 c, 32.— Vincent, 1903 a, 879, 880.— 
Walker, 1908 a, 420, 440, 443.— Weichselbaum, 1898 a, 283.— Wood & Fitz, 

1897 a, 321.— Ziegler, 1895 a, 717, fig. 445 ; 1895 c, 563, 564, 565, fig. 445 ; 

1898 a, 715, 716, fig. 531; 1899 a, 570, 571, fig. 531; 1901 a, 720, fig. 514; 
1903 a, 680, fig. 514 ; 1905, 723, 724, fig. 524 ; 1908 a, 6S9, fig. 524. 

dysenterica Pfeiffer, L., 1888 c, 662.— Axisa, 1910, 668.— Booth, 1908, 341.— 
Cayley, 1893, 630.— Delafield & Prudden, 1901, 128.— Fenoglio, 1904, 251 
(dissenterica).— Goldsmith, 1901 a, 372-374— Ha rtsock, 1904 a, 108 — 
Kartulis, 1893 a, 12.— Krouse, 1910, 269-270.— Musser & Willard, 1S93 a, 
528; 1893, 103.— Nydegger, 1907, 11-15.— Phoustanos, 1906, 68.— Posner, 
1893 a, 166; 1893 c, 674.— Potherat, 1911, 94.— Rho, 1894 a, 25, 101 (dis- 
senterica ) .—Rogers, 1902 m, 848, 849; 1903 s, 1316, 1317; 1908, 1246.— 
Stiles, 1905 e, 295, 297.— Tuttle, 1903 a, 812.— Walker, 1908 a, 405, 440, 
443.— Young, G. B., 1903, 242. 

enterica Walker, 1908 a, 429, 430, 443-444, pi. 23, fig. 9.— Gedoelst, 1911, 33. 

febris flavae Thayer, A. E., 1907 a, 45-49, figs. 1-2. 

febris tertianae Kruse, W. A. K., 1896 a, 673. 

fecalis Walker, 1908 a, 386, 387, 389, 393, 427, 429, 430, 444, pi. 24, figs. .13, 
14 —Gedoelst 1911, 33.— Wuelker, 1911, 579 (faecalis). 

felis Quincke & Roos, 1893 a, 1093.— Cramer, 1896 a, 143.— Fenoglio, 1904, 
247.— Flexner, 1901, 309.— Graser, 1900, 434 (fellis).— Gross, 1903, 432, 
433, 435, 436.— Janowski, 1897 c, 195, 198.— Messineo, 1911, 241.— Quincke, 

1899 a, 1002, 1033, 1034. 

foliata Casn grand! & P,u rbagallo, 1897 a, 586.— Wuelker, 1911, 609. 
gallopavonis Walker, 1908 a, 429, 444, pi. 24, fig. 15.— Gedoelst, 1911, 33. 


Amoeba — Continued. 

gingivalis Gros, 1849 a, 666, pi. 6, fig. C (gengivalis). — Blanchard, 1896 b, 
667-668.— Braun, 1805 b, 44; 1903, 38; 1906, 37; 1908, 42.— Brumpt, 1910, 
32.— Craig, 1911, 37.— Doflein, 1901 a, 31; 1911, 595.— Doflein & von 
Prowazek, 1903, 927.— Duval & Lemarchal, 1910, 319.— Futcher, 1903 d, 
INI.— Gedoelst, 1911, 31.— Guiart, 1910, 137, 139, 257.— Monies, 1896 a, 
17.— Neveu-Lemaire, 1902 a, 6, 9; 1904 a, 6, 9.— Schneidemuehl, 1896 a, 
259.— Stiles, 1905 e, 296 (gengivalis).— Tanaka, 1903, 5 (gingivulis).— 
Verdun, 1907 a, 41.— Walker, 1908 a, 423, 444. 

guttula Celli & Fiocca, 1894 b, 436; 1894 e, 331, 332; 1895 d, 310.— Blan- 
chard, 1896 b, 656.— Booth, 1908, 341.— Braun, 1903, 38; 1908, 35.— 
Casagrandi & Barbagallo, 1897, 140, 147; 1897 a, 580, 586, 587.— Celli, 
1896 b, 538.— Cramer, 1896 a, 142.— Doflein, 1907, 256, 257.— Doflein & von 
Prowazek, 1903, 908, 913.— Gedoelst, 1911, 31.— Glaeser, 1912, 52, 91, 92.— 
Janowski, 1897 c, 240, 241.— Kruse, W. A. K., 1896 a, 682.— Leidy, 1879 
a, 47.— Manson, 1904 a, 394; 1907, 444.— Moniez, 1896 a, 13, 14, 15.— 
Penard, 1909, 264.— Phoustanos, 1906, 68.— Rbumbler, 1898, 118, 126, 139; 
1905 c, 45.— Schneider, K. C, 1905 a, 23, 28, 29, 32, 33.— Schouteden, 

1905 a, 328.— Valilkainnf, 1905 a, 202, 203.— Verdun, 1907 a, 29 — 
Walker, 1908 a, 440.— Weicbselbaum, 1898 a, 295.— Wuelker, 1911, 609. 

histolytica (Schaudinn, 1903 a) Broido, 1903, 827, 828.— Boas, 1911, 121.— 
Castellani, 1904, 509 (histolitica).— Charles, 1908, 1254.— Dopter, 1910, 
200.— Duncan, 1912, 151.— Flexner, 1907, 535; 1909, 535.— Garin, 1910, 
397, 398; 1911, 421 (histoltica) ; 1911, 21 (histoltica).— Huber, 1909, 265, 
266, 268, 270.— Huber, J. Ch., 1906, 1609.— Jelks, 1910, 55 (hystolytica).— 
Juergens, 1906, 1607; 1907, 246.— Kraus, 1906, 1609.— Lehmann, 1912, 
591.— Martini, 1910, 390.— Meyer, 1906, 1328.— Minchin, 1907, 18, 20, 21, 
fig. 2; 1909, 18, 20. 21, fig. 2.— Motas, 1906, 682 (histoltica).— Rist, 1907, 
913.— Rogers, 1912, 1424-1425.— Ruff er & Willmore, 1909, 862.— Ruge, 

1906 b, 5, fig. 1, pi. 1, figs. 1, 2, pi. 2, figs. 1-2.— Skshivan & Stefanski, 
1908, 372, 374, 376.— Smith, A. J., & Weidman, 1910, 286.— Viereck, 1907 c, 
9, 10, 13.— Vincent, 1907, 174.— Weidner, 1910, 1148 (histologica).— Whit- 
tington, 1912, 343 (hystolytica). 

hominis (Casagrandi & Barbagallo, 1897) Walker, 1908 a, 429, 432, 444-445; 
1911, 263. 

hydroxena Entz, 1912, 19-47. 

incapsulata Wesener, 1892 a, 541 ; 1892, 551. 

intestinale Perroncito, 1894, 859. 

intestinalis Blanchard, 1885 g, 15; 1896 b, 658.— Braun, 1895 b, 42; 1903, 
37; 1908, 35.— Dock, 1902 a, 619.— Guiart, 1910, 142.— Moniez, 1896 a, 8 — 
Ruge, 1906. b, 5.— Spalikowski, 1897 a, 1056.— Stiles, 1905 e, 295, 297.— 
Verdun, 1907 a, 30. 

intestinalis Walker, 1908 a, 391, 392, 413, 414, 427, 428, 429, 430, 432, 433, 
434, 441, 445, pi. 23, fig. 8.— Doflein, 1909, 508.— Gedoelst, 1911, 33.— Smith, 
" Theo., 1910, 430, 431.— Williams, 1911, 268, 271, 273, 275, 276, 277, 280.— 
Williams & Gurley, 1910, 244, 245. 

intestinalis vulgaris Eichhorst, 1901 a, 292. — Vincent, 1903 a, 880. 

intestini vulgaris Quincke & Roos, 1893 a, 1093, 1094. — Barbagallo, 1905, 
73.— Borini, 1904, 15.— Braun, 1895 b, 41, 42; 1903, 37, 38; 1908, 35.— 
Broido, 1903, 824.— Casagrandi & Barbagallo, 1897, 110, 14S.— Craig, 1905, 
854; 1908, 329; 1911, 30.— Cramer, 1896 a, 141.— Dock, 1902 a, 619.— 
Doflein & von Prowazek, 1903, 911.— Fajardo, 1896 a, 755.— Funkhouser, 
1903, 343 (intestime vulgaris).— Futcher, 1903 d, 481.— Guiart, 1910, 141.— 
Jaeger, 1902 e, 866.— Jensen, 189S a, 134.— Messineo, 1911, 241.— Moniez, 


Amoeba — Continued. 

intestini vulgaris — Continued. 

1896 a, 6.— Prues, 1905, 27, 39.— Roos, 1894 c, 391, 398, 399.— Schneide- 
muehl, 1896 a, 258.— Steffenhagen, 1903 a, 22, 23.— Stengel, 1898, 109 — 
Stiles, 1905 e, 295.— Tanaka, 1903, 16 (vulgalis).— Verdun, 1904 f, 387, 
391 ; 1905 a, 58 ; 1907 a, 29.— Walker, 1908 a, 422, 430, 440, 445.— Weichsel- 
baum, 1898 a, 283.— Zoru, 1901 a, 12 ; 1902 a, 371. 

istolitica Fenoglio, 1904, 251, 252. 

jelaginia von Mereschkowsky, 1878 a, 204, pi. 11, figs. 29-30. — Braun, 1895 b, 
43.— Leuckart, 18S6d, 189.— Moniez, 1896 a, 9.— Railliet, 1885 a, 150. 

kartulisi Doflein, 1901 a, 30-31.— Braun, 1903, 40, fig. 5; 1906, 38, fig. 5; 
1908, 42, fig. 6.— Brumpt, 1910, 33.— Chatton, 1910, 247.— Doflein & von 
Prowazek, 1903, 924.— Duval & Lema renal, 1910, 319.— Gedoelst, 1911, 
32.— Guiart, 1910, 139.— Hickson, 1909, 84.— Kaestner, 1906, 11.— Stiles, 
1905 e, 296.— Verdun, 1907 a, 44, fig. 6.— Walker, 1908 a, 423, 445. 

lacertae Hartmann in Hartmann & von Prowazek, 1907, 314, 315, 320, fig. 
4 f— Braun & Luehe, 1909, 19.— Chatton, 1910, 252; 1910, 304, 316.— 
Chatton & Lalung-Bonnaire, 1912, 140, 141.— Doflein, 1909, 513, fig. 454; 
1911, 573, 583, fig. 516.— Glaeser, 1912, 97.— Hartmann, 1911, 6, fig. 1.— 
Hartmann & Naegler, 1908, 113.— von Janicki, 1909, 392.— Kisskalt & 
Hartmann, 1910, 18-19, fig. 1.— Naegler, 1909, 19-20, 24, 31, 32, 38, 40, 
pi. 1, figs. 8-13, pi. 2, figs. 45-52.— Popoff, 1911, 209, 217.— Whitmore, 1911, 
78.— Wuelker, 1911, 610. 

lagopodis Fantham, 1910, 702-703, pi. 61, figs. 58-65 ; 1910, 30. 

letullei Neveu-Leroaire, 1912, 189.— Letulle, 1908, 256-266, figs. 1-6, pi. 4, 
figs. 1-3. 

Umax Pfeiffer, L., 1891 a, 211, fig. 88 b.— Craig, 1911, 190, 191, fig. 26 — 
Doflein, 1907, 256, 257, 270.— Greig & Wells, 1911, 53.— Guiart, 1911, 849, 
figs. 2, 3.— Schneider, K. C, 1905 a, 23, 32.— Werner, 1908 e, 433, 434, 435 
(15, 16, 17), figs. 36-38; 1909, 244, 245, figs. 36-38.— Williams & Gurley, 
1910, 245, 246. 

lobosa Celli & Fiocca, 1894 b, 435, 436, 440 ; 1894 e, 321.— Blanchard, 1896 b, 
656.— Fajardo, 1896 a, 755.— Gedoelst, 1911, 31.— Janowski, 1897 c, 240, 
242.— Moniez, 1896 a, 12, 13, 14.— Neveu-Lemaire, 1912, 197.— Pru&s, 1905, 
27.— Stiles, 1905 e, 295.— Strong, L. W., 1898 a, 257.— Tsujitani, 1898 a, 
666, 667.— Walker, 1908 a, 440. 

lobosa coli Celli & Fiocca, 1894 b, 436; 1894 e, 333, 338.— Braun, 1903, 38; 
1908, 35.— Moniez, 1896 a, 13.— Stiles, 1905 e, 295.— Verdun, 1904 f, 388; 

1907 a, 29.— Walker, 1908 a, 430, 431, 440, 446. 
lobosa gruberi Wuelker, 1911, 592, 609. 

lobosa guttula Celli & Fiocca, 1894 b, 436; 1894 e, 331-332, 338.— Braun, 
1903, 38; 1908, 35.— Craig, 1908, 329 (guttata); 1911, 32 (guttata).— 
Doflein & von Prowazek, 1903, 912.— Janowski, 1897 c, 239.— Moniez, 
1896 a, 13.— PruSs, 1905, 27.— Stiles, 1905 e, 295.— Strong, R. P., 1907 a, 
494.— Verdun, 1907 a, 29.— Walker, 1908 a, 430, 431, 440, 445. 

lobosa oblonga Celli & Fiocca, 1894 b, 436; 1894 e, 332, 338.— Braun, 1903, 
38; 1908, 35.— Craig, 1908, 329; 1911, 32.— Doflein & von Prowazek, 1903, 
912.— Janowski, 1897 c, 239.— Moniez, 1896 a, 13.— Pru6s, 1905, 27.— Stiles, 
1905 e, 295.— Strong; R. P., 1907 a, 494.— Verdun, 1907 a, 29.— Walker, 

1908 a, 430, 431, 440, 446. 

lobospinosa Craig, 1912, 1, 25-30, 31, pi. 2, fig. 4, lower group. 

malaria? (Laveran, 1880) Sakharov, 1892 a.— Weichselbaum, 1898 a, 291. 

malaria? febris quartanae Kruse, W. A. K., 1896 a, 672. 


Amoeba — Continued . 

meleagridis Smith, Theo., 1895 a, 1-38, pis. 1-5.— Buchanan, R. E., 1911, 
41C— Cole, 1908, 297-298 (melegridis).— Cole & Hadley, 1910, 918-919.— 
Crawley, 1912, 484.— Curtice, 1907, 5-04; 1907, 67-105.— Doflein, 1909, 
508.— Fantham, 1910, 703.— Gedoelst, 1911, 32.— Hadley & Amison, 1911, 
34-41.— Hassall, 1890 b, 1.— Kaestner, 1906, 12.— Kaupp, 1911, 410-416, 
fig. 3.— Kruse, W. A. K., 1896 a, 618.— Laveran & Lucet, 1905 a, 676.— 
Milks, 1908, 3-7.— Neveu-Lemaire, 1912, 193.— Smith, Theo., 1910, 509- 
512.— Walker, 1908 a, 424, 446 (meliagridis).— Watanabe, 1910, 67-81. 

minuta (Elmassian, 1909) Gedoelst, 1911, 33. 

mitts Cramer, 1896 a, 143.— Graser, 1900, 434.— Janowski, 1897 c, 194, 195, 
198.— Quincke, 1899 a, 1033. 

miurai Ijima, 1898 a, 85-94, figs. 1-9.— Braun, 1903, 41, fig. 6; 1906, 39, 
fig. 6; 1908, 44, fig. 7.— Bruinpt, 1910, 34.— Craig, 1911, 37.— Doflein, 1909, 
516-517, fig. 457 ; 1911, 586, fig. 519.— Doflein & von Prowazek, 1903, 925 — 
Gedoelst, 1911, 32, fig. 32.— Guiart, 1910, 153-154, 257, fig. 118.— Neveu- 
Lemaire, 1902 a, 6, 9; 1904 a, 6, 11.— Seifert, 1908 a, 485.— Verdun, 1907 a, 
42.— Walker, 1908 a, 423, 446. 

mortinatalium (Smith & Weidman, 1910) Gedoelst, 1911, 33. 

mucicola Chatton, 1909, 690-692 ; 1910, 247-262 ; 1910, 267, 270, 272, 274, 275, 
277, 280, 315, 316.— Chatton & Lalung-Bonnaire, 1912, 138, 141.— Doflein, 
1911, 573.— Glaeser, 1912, 139. 

muris Grassi, 1882 a, 181-182.— de Beaurepaire Aragao, 1909, 36.— Braun, 

1895 b, 43.— Doflein, 1901 a, 18; 1907, 281; 1909, 496, 497; 1911, 595.— 
Keysselitz, 1908, 259.— Schepotieff, 1910, 496, 498.— Schneidemuehl, 1896 a, 
259.— Stiles & Hassall, 1910 b, 115, 121.— Walker, 1908 a, 424, 427. 429, 
431, 433, 434, 435, 446, pi. 24, fig. 12.— Wenyon, 1907 i, 170-180, 183. 187, 
1 fig., pi. 10, figs. 1-37.— Werner, 1911, 73. 

musculi Walker, 1908 a, 429, 441, 447, pi. 23, fig. 11. 
nipponica (Koidzumi, 1909) Gedoelst, 1911, 33. 

oblonga Celli & Fiocca, 1894 b, 436; 1894 e, 332; 1S95 d, 310.— Behla, 
1898 b, 31.— Blanchard, 1896 b, 656.— Booth, 1908, 341.— Braun. 1903, 38; 

1905, 35.— Casagrandi & Barbagallo, 1897, 140, 147; 1897 a, 5S6.— Celli, 

1896 b, 538.— Cramer, 1896 a, 142.— Gedoelst, 1911, 31.— Janowski, 1897 c, 
241.— Manson, 1904, 394 ; 1907, 444.— Moniez, 1896 a, 13, 15.— Phoustanos, 

1906, 68.— Vahlkampf, 1905 a, 202, 203, 204.— Verdun, 1907 a, 29.— 
Wuelker, 1911, 609. 

paedophthora, Caullery, 1906, 266-269, figs. 1^.— Chatton, 1909, 690 (pae- 
dophtora) ; 1910, 248 (poedophtora). — Chatton & Lalung-Bonnaire, 1912, 
141 (poedophtora).— Doflein, 1909, 515, fig. 456; 1911, 585, fig. 518 — 
Glaeser, 1912, 75. 

parasitica von Lendenfeld, 1885 a, 35-38, pi. 6, figs. 1-4.— Chatton, 1910, 
247.— Doflein, 1909, 515-516; 1911, 585.— Fiebiger, 1912, 76.— Gedoelst, 
1911, 31.— Grassi, 1888 e, 89.— Kruse, W. A. K., 1896 a, 699.— Motas, 1906. 
6S2-6S3.— Neveu-Lemaire, 1912, 193.— Railliet, 1S85 a, 150-151; 1893 a, 

phagocyto'ides (Gauducheau, 1907) Gedoelst, 1911, 32. 

pigmentifera Grassi, 1881, 354. — Casagrandi & Barbagallo, 1897, 140. — 
Doflein, 1901 a, 20.— Grassi, 1882 a, 185-187, pi. 4, figs. 1, 2, 7, 8, 9, 10, 
11, 12-26, 28-43.— Labbe\ 1899 a, 126, fig. 196.— Pfeiffer, L., 188S c, 660, 
665, pi. 10, figs. 12-43.— Schepotieff, 1910, 496.— Schubotz. 1905 b, 4.— 
Stengel, 1S91 b, 223.— Walker, 190S a, 404. 

pulmonalis Artault, 1898, 275-277, 299.— Braun, 1903, 39; 1906, 37; 190S, 
43.— Brumpt, 1910, 33.— Craig, 1911, 37.— Doflein, 1911, 595.— Doflein & 


Amoeba — Continued . 

pulmon&lis Artault — Continued. 

von Prowazek, 1903, 927.— Gedoelst, 1911, 32.— Guiart, 1910, 152.— Neveu- 
Leinaire, 1002 a, 6, 9; 1904 a, 6, 9.— Seifert, 1908 a, 485.— Verdun, 1907 a, 
41-42.— Walker, 1908 a, 423, 447. 

ranae (Hartinann, 1907) Walker, 1908 a, 426, 429, 447, pi. 24, fig. 16. 

ranarum Grassi, 1879 n, 446.— de Bonis, 1882 a, 146.— Dobell, 1909, 245.— 
Doflein, 1901 a, 1S-19.— Grassi, 1882 a, 182-183.— Perroncito, 1882 a, 
86.— Schneider, K. C., 1905 a, 28, 29, 33, 34, pi. 2, fig. 7.— Walker, 190S a, 
424, 447-44S. 

reticularis Celli & Fiocca, 1894 b, 435, 439, 440; 1S94 e, 330, 336, 338.— 
Blanchard, 1896 b, 656.— Booth, 1908, 341.— Borini, 1904, 15.— Braun, 
1903, 3S; 1908, 35.— Casagrandi & Barbagallo, 1897, 140, 147, 151.— Celli 
& Fioccn, 1895 d, 310.— Craig, 1908, 329; 1911, 32.— Doflein & von Prowa- 
zek, 1903, 912.— Gedoelst, 1911, 32.— Janowski, 1897 c, 239, 240, 241.— 
Manson, 1904, 394; 1907, 444.— Moniez, 1896 a, 12, 13, 14.— Phoustanos, 
1906, 68.— Prues, 1905, 27.— Stiles, 3905 e, 295.— Strong, R. P., 1907 a, 
495.— Verdun, 1907 a, 29.— Walker, 1908 a, 430, 431, 448. 

rotatoria Mayer, 1843 a, 11-12, pi. 3, fig. 11.— Braun, 1908, 61.— Castellani 
& Chalmers. 1910, 270.— Davaine, 1877 a, xvii.— Dofiein, 1909, 362 ; 1911, 
420.— Franga & Athias, 1906, 127, 131, 135, 138, 139, 142, 147.— Lebedeff, 
1910, 404, 430.— Mnnson, 1907, 846.— Musgrave & Clegg, 1903 a, 50 (rota- 
tori urn p. 20).— von Siebold, 1850 c, 649.— Ziegler, 1885 c, 346. 

sagittae Grassi, 18S1, 354.— Doflein, 1901 a, 20.— Labbe, 1899 a, 126.— Porter, 
1909, 40.— Sehepotieff, 1910, 496.— Schubotz, 1905 b, 4.— Walker, 1908 a, 

404 (sagettne). 

sp. Blanc, 1899 c, 87-89. 

sp. Chatton, 1910, 348. 

sp. Kunstler, 1S88 b, 955. 

sp. Rentsch, 1S60 a, 14, 63-66, pi. 8, fig. 7 h, pi. 15, fig. 2 u-w. 

sp. Schneider, A. C. J., 1875 f, 603, pi. 22, figs. 81-84 ; 1876 a, 72, 115, pi. 22, 
figs. 81-84. 

sp. Shipley, 1898 d. 11-12. 

sp. Wenyon, 1907 i, 181-184, pi. 12, figs. 25-30, pi. 10, figs. 38-41. 51. 

spinosa Celli & Fiocca, 1894 b, 435. 437, 438, 440 ; 1894 e, 330, 333-334, 335, 
338.— Behla, 1898 b, 31.— Blanchard, 1896 b, 656.— Booth, 1908, 341.— 
Borini, 1904, 15.— Braun, 1903, 38; 1908, 35.— Casagrandi & Barbagallo, 
1897, 140, 147, 151; 1897 a, 586, 587.— Celli, 1896 b, 538.— Celli & Fiocca, 

1895 d, 310.— Craig, 1908, 329; 1911, 32.— Doflein & von Prowazek, 1903, 
912.— Gedoelst, 1911, 32.— Janowski, 1897 c, 239, 240, 241, 242.— Moniez, 

1896 a. 12, 13, 14.— Neveu-Lemaire, 1912, 197.— Phoustanos, 1906, 68.— 
Prues, 1905, 27.— Stiles, 1905 e, 295.— Strong, L. W., 1898 a, 257.— Strong, 
R. P., 1907 a, 495.— Tsujitani, 1898 a, 667.— Vahlkampf, 1905 a, 202. 203, 
204.— Verdun, 1907 a, 29.— Walker, 1908 a, 430, 431, 448.— Williams, 1911, 
204 (apinoza).— Wuelker, 1911, 609. 

succinea Pfeiffer, L., 1891 a, 211, fig. 88 c. 

tetraycna (Viereck, 1907) Bertarelli, 1912, 50.— Brumpt, 1910, 31-32.— 
Carini, 1912, 218.— Chagas, 1911, 137.— Garin, 1910, 398.— Gedoelst, 1911, 
33, fig. 33.— Hartman, 1908, 126 [226].— Huber, 1909, 270.— Kuenen. 1909, 
651.— Williams, 1911, 27<>. 

tropicalis (Lesage, 1908) Gedoelst, 1911, 33. 

undulans Cell! & Fiocca, 1894b, 435, 436.— Brumpt, 1910, 142.— Cassagrandi 
<fc Barbagallo, 1897, MO. — Celli, 1896 b, 538.— Gedoelst, 1911, 32.— Vahl- 
kampf. 1905 a, 202.— Verdun, 1907 a, 32-33. 


Amoeba — Continued . 

urogenital Baelz, 1883 a, 237.— Braun, 1895 b, 44^6; 1903, 31); 1906, 37; 
1908, 43.— Bruinpt, 1910, 33.— Craig, 1911, 37.— Doflein, 1901 a, 80.— 
Doflein & von Prowazek, 1903, 924.— Dunglison, L893 a, 48. — Futcber, L903 
d, 481.— Gedoelst, 1911, 31.— Guiart, 1910, L52, 257.- -Hickson, L909, 81.— 
Ijima, 18S9 b, 57.— Kaestaer, L906, 11.— Kartulis, L906, 354.— Moniez, 
1896 a, 15-16.— Neveu-Lema ire, 1902 a, G, 9; 1904 a, o. 9.— Poaner, 1893 c, 
675.— Seifent, 1908 a, 485.— Stengel, 1892 a, 291. — Stiles. 1905 e, 296.— 
Tanaka, 1903, 5.— Verdun, 1907 a, 41.— Walker, 1908 a, 423, 448. 

vaginalis Blanchard, 1885 g, 15.— Brumpt, 1910, 33.— Guiart, 1910, 152.— 
Moniez, 1896 a, 15.— Raillict, 1893 a, 118.— Spalikowflki, 1897 a, L056.— 
Stiles, 1905 e, 296.— Verdun, 1907 a, 41. 

vermicularis Celli & Fiocca, 1894 b, 435, 438, 440; 1S94 e, 331, 335-336, 338; 
1895 d, 310.— Blanchard, 1896 b, 656.— Booth, 1908, 341.— Borini, 1904, 
15.— Braun, 1903, 38; 1908, 35.— Casagrandi & Barbagallo, 1897, 140, 147, 
151.— Celli, 1896 b, 538.— Craig, 1908, 329; 1911, 32.— Doflein & von Pro- 
wazek, 1903, 912.— Gedoelst, 1911, 32.— Janowski, 1897 c, 239, 242.— 
Manson, 1904, 394; 1907, 444.— Moniez, 1896 a, 13, 14— Phoustanos, 1900, 
68.— Prues, 1905, 27.— Stiles, 1905 e, 295.— Strong, II. P., 1907 a, 495.— 
Vahlkampf, 1905 a, 202.— Verdun, 1907 a, 29.— Walker, 1908 a, 430, 431, 

viridis Wuelker, 1911, 609. 

vulgaris Boos, 1894 c, 391, 405.— Artault, 1898, 275, 276.— Casagrandi & 
Barbagallo, 1897 a, 579.— Cramer, 1896 a, 143.— Flexner, 1907, 532 ; 1909, 
532.— Glaeser, 1912, 31.— Gross, 1903, 432, 435, 436, 437, 438, 445.— Janow- 
ski, 1897 c, 194, 234.— Ruge, 1906 b, 3, 11.— Shiga, 1898, 819. 
Endamoeba Leidy, 1879 k, 205 ; 1904 a, 150 ; 1905 a, 156.— Chatton, 1912, 111.— 
Hickson, 1909, 82. 

blattae (Buetschli, 1878) Leidy, 1879 a, 300; 1879 k, 205; 1904 a, 156-157; 
1905 a, 156-157. 
• coli (Loesch, 1875) Hickson, 1909, 82.— Schubotz, 1905 b, 34. 

histolytica (Schaudinn, 1903) Hickson, 1909, 82, 83.— Schubotz, 1905 b, 34 

miurai (Ijima, 1898) Hickson, 1909, 83 (iurai). 

undulans Hickson, 1909, 83. 
Entamoeba Casagrandi & Barbagallo, 1897, 163.— Alexeieff, 1912, 70.— Braun, 

1908, 35.— Buchanan, R. E., 1911, 416.— Calkins, 1909, 295.— Castellan! & 
Chalmers, 1910, 214.— Chatton, 1912, 110, 111, 114.— Craig, 1911, 20, 26. 29, 
33, 34, 35, 36, 37.— Crawley, 1912, 484.— Doflein, 1909, 156, 221, 491-509.— 
Gauducheau, 1909, 251.— Guiart, 1910, 141.— von Prowazek, 1911, 345-350 ; 
1912, 273-274.— Schaudinn, 1903 a, 547-576.— Sluiter & Swellengrebel, 
1912, 20-27, 164.— Verdun, 1907 a, 29.— Walker, 1908 a, 440. 

africana Hartmann in Hartmann & von Prowazek, 1907, 312, 320, fig. 6. — 
Buchanan, R. E., 1911, 422.— Castellani & Chalmers, 1910, 221.— Chatton, 
1910, 284.— Craig, 1911, 180; 1911, 363; 1912, 2.— Dobell, 1909, 254.— Dock, 

1909, 85.— Doflein, 1909, 21, 495, fig. 17; 1911, 577.— Elmassian, 1909, 
335.— Fantham, 1911, 114.— Hartmann, 1908, 117-127 [217-227] ; 1909, 
209; 1911 51.— Koidzumi, 1909, 650.— Walker, 1911, 262.— Werner, 1909, 
241.— Whitmore, 1912. 516. 

apis Fantham & Porter, 1911, 626 ; 1912, 138. 

aulastomi Noeller, 1912, 195-199, pi. 19, figs. 1-22. 

blattae (Buetschli, 1878).— Alexeieff, 1912, 69, 70, 71 : 1912, 156; 1912, 105 — 

Castellani & Chalmers, 1910, 215.— Chatton, 1910, 283. 289, 290 fig. 5 za-ze; 

1912, 110-111.— Dobell, 1909, 246.— Doflein, 1909, 499; 1911, 598, 599, fig. 


Entamoeba — Continued. 

blattae — Continued. 

529.— Glaeser, 1912, 30, 113, 114.— Hartmann, 1909, 219 ; 1910, 4, 5, 7, 8, 9 ; 
1911, 16.— Hartmann & Chagas, 1910, 164.— Hartmann & Whitmore, 1912, 
192.— Hickson, 1909, 83, fig. 17.— von Janicki, 1909, 381-393, figs. l-7b.-^ 
Mercier, 1910, 143-175, figs. 1-6, pis. 10-12, figs. 1-63.— Popoff, 1911, 210.— 
Wuelker, 1911, 594. 

Mattarum Casagrandi & Barbagallo, 1897, 163.— Hartmann, 1911, 58; 1912, 

bovis (Liebetanz, 1905).— Doflein, 1909, 499; 1911, 598— Fiebiger, 1912, 76. 

Mccalis (Steinberg, 1862).— Braun, 1908, 41, fig. 41.— Braun & Luehe, 1909, 
17, fig. 1 ; 1910, 18, 21, fig. 1.— Castellani & Cbalmers, 1910, 214-215, 222, 
232, 925.— Chatton, 1910, 247; 1910, 268, 284, 285, 304, 315, fig. 5 g-k.— 
Craig, 1911, 10, 36, 230-232, 235, fig. 30.— Daniels & Wilkinson, 1909, 221.— 
Doflein, 1907, 278 ; 1909, 506, 507, figs. 448, 449 ; 1911, 594, figs. 523, 524.— 
Erdmann, 1910, 335.— Froscb, 1909, 191.— Glaeser, 1912, 30, 90, 104 — 
Guiart, 1910, 138.— Hartmann, 1909, 209 ; 1910, 8, 9.— Hartmann & Chagas, 
1910, 112.— Hartmann & von Prowazek, 1907, 313, 316, fig. 5.— von Janicki, 
1909, 392.— Kartulis, 1906, 354.— Keysselitz, 1908, 345.— Kisskalt & Hart- 
mann, 1907, 105, 107, 113; 1910, 16, 21-23, 27, 29, figs. 4, 5.— Koidzumi, 

1909, 653.— Levander, 1908, 49-50.— von Leyden & Loewentbal, 1905 a, 
3-11, pi. 1, figs. 1-12.— Loewentbal & von Rutkowski, 1907, 393.— Mercier, 

1910, 147.— Naegler, 1909, 26, 45.— Perroncito, 1882 a, 86.— Popoff, 1911, 
210, 216.— von Prowazek, 1904 1, 42-44 ; 1910, 149.— Seifert, 1908 a, 485.— 
Sistrunk, 1911, 1508.— Sluiter & Swellengrebel, 1912, 26.— Smith & Weid- 
man, 1910, 295, 297.— Stitt, 1909, 173, 176 ; 1910, 190, 193.— Tietze, 1905 a, 
304.— Verdun, 1907 a, 41.— Walker, 1908 a, 423, 448-449. 

luetschlii von Prowazek, 1912, 243, 245-246. 

cochincJiinensis Sluiter & Swellengrebel, 1912, 23, 24, fig. 5. 

coli (Loesch, 1875).— Albu, 1905, 436.— Alexeieff, 1912, 105.— Allan, 1909, 
1212; 1911, 87.— Ashburn & Craig, 1907, 41, 42, 43, 140, 141, 222, 223, 
224, 225, 347, 348.— Awerinzew, 1909, 107.— Barbagallo, 1905, 73, 74, 75; 
1905, 282.— Bates, 1909, 56.— Bertarelli, 1905, 196; 1905, 398; 1912, 49, 
51.— Billet, 1907, 1233; 1907, 215.— Booth, 1908, 341, 342, 343.— Braun, 

1908, 36.— Braun & Luehe, 1909, 17, 18, 19, 20, 27, fig. 2; 1910, 18, 19, 
21.— Brem & Zeiler, 1910, 678.— Broi'do, 1903, 827, 828, 829.— Brown, 
W. C, 1912, 222, 223, 225, fig. 2.— Buchanan, It. E., 1911, 416, 418, 
fig. 186.— Calkins, 1904, 14; 1907, 366; 1907, 225, 226; 1908, 423, 426; 

1909, 116.— Castellani, 1904, 507.— Castellani & Chalmers, 1910, 206, 214- 
216, 231, 346, 925, 976.— Chapin, 1910, 88.— Chatton, 1910, 248, 261 ; 1910, 
282, 288, 306, 311; 1912, 111.— Chatton & Brodsky, 1909, 12.— Chat- 
ton & Lalung-Bonnaire, 1912, 139, 142.— Craig, 1904, 299 ; 1904, 185 ; 1905, 
244, 245, 246, 247; 1905, 854-861, 897-903, 936-942; 1906, 214, 219, 220; 
1908, 324-374; 1910, 1, 5, 10; 1911, 8, 14, 18, 22, 24, 25, 32, 34, 35, 36, 43, 
51, 60, 61, 73-113, 115, 117, 118, 120, 121, 122, 123, 124, 127, 128, 130, 132, 
133, 134, 141, 143, 164, 166, 178, 180, 181, 182, 183, 186, 193, 194, 195, 196, 
197, 198, 199, 202, 206, 212, 213, 217, 221, 228, 231, figs. 1-8 ; 1911, 362, 363, 
364, 365, 366; 1912, 1, 2, 3, 4, 5, 7-13, 15, 16, 19, 24, 30, 31, 32, pi. 1; 1912, 
3, 4, 6, 11, 12, 14.— Deeks & Shaw, 1911, 2, 3.— Dobell, 1908, 432; 1909, 
246, 247, 253; 1909, 285, 286, 288.— Dock, 1909, 84.— Doflein, 1907, 270, 279, 
280, 281 ; 1909, 148, 184, 193, 485, 491, 492, 493, 519, 853, figs. 430, 433 ; 

1911, 208, 586, fig. 213.— Doflein & von Prowazek, 1903, 912, 916, 920-921, 
figs. 33, 34, 35.— Elmassian, 1909, 335, 336, 339, 340, 343, 346, 347, 348 — 
Fantham, 1910, 703; 1911, 111-121.— Fiebiger, 1912, 74, fig. 13.— Flexner, 


Entamoeba — Continued . 
voli — Continued. 

1907, 535; 1909, 535.— Frosch, 1909, 191.— Gauducheau, 1907, 486.— Greig 
& Wells, 1911, 7, 14, 29.— Guiart, 1910, 142.— Hartmann, 1907, 141, 143, 
144, fig. A 1 ; Hartmann in Hartmann & Naegler, 1908, 113 ; Hartmann, 1908, 
117, 118, 122, 124 [217, 218, 222, 224] ; 1909, 208, 209, 211, 213; 1909, 502; 

1910, 8, 9; 1911, 50, 51, 52, 53, 54, 55, 58, 59; 1912, KM. L65, 107. L88, 171, 
173, 176, 178, 179, 180.— Hartmann & von Prowazek, 1907, 312.— Hart- 
mann & Whitmore, 1912, 182-192, figs. A-B, pis. 17-18, figs. 1-29.— Her- 
rick, 1910, 664.— Holt, 1908, 2143; 1909, 49.— von Janicki, 1908, 149, 150, 
151.— Juergens, 1907, 771, 777, 779.— Kaestner, 1906, 11.— Kartulis, 1906, 
354.— Keysselitz, 1908, 259.— Kiewiet de Jonge, 1904 a, 79, 80, 81.— King, 

1911, 183, 185, 186.— Kisskalt & Hartmann, 1907, 105, 108, 109, 112, fig. 
4; 1910, 16, 23-26, 27, 29, figs. 6-7.— Koidzumi, 1909, 650, 651, 652.— 
Kuenen, 1909, 549, 550, 552, 563, 564.— Kuscbakewitsch, 1907, 236.— Leger 
& Duboscq, 1904 f, 345.— Lebmann, 1912, 591.— Lesage, 1904 a, 1237, 1238, 
1239; 1905 a, 9, 10, 11, 13, 14, 16; 1907, 1157-1159; 1908, 104-105, 107, 
108, 110, 111, figs. 1-6.— Liston, 1911, 107.— Loewentbal, 1903, 268.— 
Luebe, 1909, 421, 423.— McCarrison, 1909, 733, 734.— Manson, 1907, 437, 
440.— Matbis & Leger, 1911, 208.— Menetrier & Touraine, 1908, 909.— 
Mercier, 1908, 942 ; 1910, 144, 164.— Metcalf, 1910, 310, 315.— Meyer, 1906, 
1327.— Motas, 1906, 682.— Musgrave & Clegg, 1906, 911, 915, 916, 917, 922, 
929, 935, 938, 939, 941, 946, 947.— Naegler, 1909, 30, 32.— Neresbeimer, 

1908, 49.— Noc, 1909, 180, 189, 190, 194, 201, pi. 11, fig. 13.— Noeller, 1912, 
196, 198, 199.— Popoff, 1911, 210, 211.— von Prowazek 1904 1, 42, 43; 

1911, 345, 347, 348, 349; 1912, 30; 1912, 273; 1912, 242, 243, 244, 245.— 
PruSs, 1905, 30, 43, 45.— Huge, 1906 b, 4, 5, 11, 13, fig. 5.— Scbaudinn, 
1903 a, 564, 565-570, 571, 572, 573, 574, 575.— Scbepotieff, 1910, 496, 498.— 
Scbubotz, 1905 b, 5, 6, 23.— Simon, C. E., 1907, 289; 1911, 215.— Simon, 
S. K., 1909, 1528.— Sistrunk, 1911, 1507, 1509.— Sluiter & Swellengrebel, 

1912, 20, 21, 22, 23, 27, 164, fig. 3.— Smitb, A. J., & Weidman, 1910, 295, 
296.— Smitb, Tbeo., 1910, 430.— Stiles, 1905 e, 296, 29S, 299-301, 302; 
1907 e, 525 ; 1911, 1276 ; 1911, 1348.— Stitt, 1910, 190, 191.— Strong, R. P., 
1907 a, 496, 498, 499, 500, 519.— Tanaka, 1910, 2300.— Tbornburgh, 1908, 
55, 56.— Vablkampf, 1905 a, 168, 210.— Vedder, 1906 a, 870-872; 1907 a, 
190-195; 1911, 51.— Verdun, 1904 f, 388; 1907 a, 29.— Viereck, 1906 e, 
1064, 1066 ; 1907 c, 9, 14, 28, 29, 30, 31, 32, figs. 1-3, 4.— Volbracbt, 1904 b, 
163.— Walker, 1908 a, 381, 383, 404, 405, 413, 422 431, 433, 439, 440, 449 ; 
1911, 260-261, 262, 263, 264, 269, 273, 274, 275, 276, pi. 4, figs. 9, 11.— 
Wallace, 1912, 689, 690, 691.— von Wasielewski, 1911, 122.— Wenyon, 
1907 i, 171, 172, 173, 174, 178, 180 ; 1908 b, 128, 129, 130. fig. 35 ; 1908 k, 
1245.— Werner, 1908 e, 425, 430 (7, 12) ; 1909, 241, 244.— Wbitmore. 1911, 
71, 72, 75, 76, 77, 78, fig. 2; 1911, 85, 93; 1911, 235; 1912, 515, 516, 517, 
518, 519.— Williams, 1911, 56-58 ; 1911, 274, 277, 279.— Williams & Gurley, 
1910, 239, 246.— Wuelker, 1911, 594, 595, 596, 597, 610.— Young, W. B., 

1910, 586. 

coli var. nipponica Walker, 1911, 279, pi. 4, fig. 10. 

dentalis (Braun, 1883).— Castellani & Cbalmers, 1910, 214, 925.— Craig, 

1911, 232.— Froscb, 1909, 191, 194.— Sluiter & Swellengrebel, 1912, 26. 
dysenteriw (Councilman & Lafleur, 1891). — Alexeieff, 1912, 105. — Asbburn & 

Craig, 1907, 41, 42, 43, 140, 222, 223, 224, 225, 347.— Craig, 1905, 245-298, 
figs. 1-4, pi. 1, figs. 1-12; 1905, 854-861, 897-903, 936-942; 1006, 214, 
219.— Doflein, 1911, 580, 58S— Gauducbeau, 1907, 487.— Holt, 1908, 2143; 

1909, 49.— Lebmann, 1912, 591.— Musgrave & Clegg, 1906, 935.— Simon, 


Entamoeba — Continued. 

dy sentence — Continued. 

C. E., 1907, 286; 1911, 213.— Vedder, 1906 a, 870, 872; 1907 a, 190-195; 
1911, 51. 

dysenterica (Pfeiffer, 1888).— Thornburgh, 1908, 55, 56. 

gingicalis (Braun, 1895).— Castellani & Chalmers, 1910, 214, 925.— Craig, 
1911, 232.— Sluiter & Swellengrebel, 1912, 26. 

1i artni an ni von Prowazek, 1912, 243-245. 

histolytica Scbaudinn, 1903 a, 564, 570-576.— Acbard, 1911, 179.— Albu, 1905, 
436.— Albu & Werzberg, 1912, 396.— Allan, 1909, 145 (bistolitica) ; 1909, 
1212, 1213; 1910, 63; 1910, 1092; 1910, 181-183; 1911, 87.— Anderson, 
1908, 1243, 1244.— Asbburn & Craig, 1907, 347, 348.— Balfour, 1911, 367; 
Barbagallo, 1905, 73-75; 1905, 282; 1905, 145, 146; 1906, 380, 381 — 
Basseres, 1911, 256.— Bates, 1909, 56.— Bertarelli, 1905, 196, 197, 198 
(bystolitica) ; 1905, 398, 399; 1912, 49, 50 (bystolitica).— Billet 1905. 
874-S76; 1907, 1233; 1907, 215, 216, 217.— Blackbam, 1908, 77.— Booth, 
190S, 341, 342, 343 (bistolitica).— Bra u, 1908, 512, 513.— Braun, 1908, 
37.— Braun & Luehe, 1909, 20; 1910, 21, 22.— Brem & Zeiler, 1910, 675, 
677, 678, 679, 680, 682, 683.— Brown, W. C, 1912, 221, 222, 223, 224. 
225, fig. 1.— Brumpt, 1910, 20.— Buchanan, R. E., 1911, 416, 419, 420, 
fig. 187.— Calkins, 1904, 14; 1907, 366.— Castellani, 1904, 507, 508 (bis- 
tolitica ) ; 1905, 67, 69.— Castellani & Chalmers, 1910, 11, 205-206, 214- 
215, 217, 232, 669, 925, 976, 982, 1012, 1015-1016.— Chamberlain & Vedder, 

1911, 384.— Chantemesse & Rodriguez, 1909, 31 ( hystoly tica ) .— Chapin, 
1910, 88.— Cbatton, 1910, 284, 288, 306, fig. 5 a-f.— Chatton & Lalung- 
Bonnaire, 1912, 139.— Chlapowski, 1909, 86, 87, 326.— Cooke, 1910, 598; 
1910, 325.— Craig, 1904, 299; 1904, 185, 186; 1905, 244, 245; 1905, 855; 

1908, 324-374; 1910, 1, 5, 10; 1911, 2, 6, 9, 14, 17, 19, 22, 23, 24, 25, 
34, 35, 36, 43, 51, 59, 60, 61, 63, 73, 77, 78, 81, 84, 87, 88, 89, 90, 92, 
93, 97, 99, 110, 114-179, 180, 181, 183, 184, 185, 186, 187, 189, 190, 191, 
192, 193, 194, 195, 196, 197, 19S, 199, 200, 202, 205, 207, 209, 212, 213, 215, 
217, 221, 227, 228, 231, 233, 235, figs. 9-21 ; 1911, 362, 363, 364, 365, 366 ; 

1912, 1, 2, 4, 5, 13-20, 21, 23, 24, 25, 30, 32, pi. 2 ; 1912, 3, 4, 11, 12, 13.— 
Daniels & Stanton, 1907, 354.— Daniels & Wilkinson, 1909, 221.— Deeks & 
Shaw, 1911, 2, 3, 4, 5, 7, 11, 22.— Dobel, 1909, 285.— Dock, 1909, 84.— 
Doflein, 1909, 126, 500, 501, 502, 503, 519, 520, 521, figs. 440, 441, 442, 443, 
444, 445, 446; 1911, 137.— Doflein & von Prowazek, 1903, 921-922, fig. 38 
(bystolytica).— Dopter, 1905, 417; 1910, 124, 126.— Elmassian, 1909, 336, 
339, 340, 348.— Fantham, 1910, 703; 1911, 113, 116, 117, US.— Fiebiger, 
1912, 75, fig. 15.— Flexner, 1907, 535; 1909, 535.— Gauducbeau, 1907, 486, 
487.— Glaeser, 1912, 113.— Greig & Wells, 1911, 7, 14, 18, 19, 29.— Guiart, 
1910, 142, 143.— Hartmann, 1907, 144: 1908, 118, 125, 126 [218, 225, 226] ; 

1909, 207-220, pi. 13, figs. 1-25; 1909, 502; 1910, 7, 8, 9 ; 1911, 50, 51, 52, 
53, 54, 55, 56, 58-64, figs. 27-36; 1912, 163, 164, 166, 167, 171, 174, 178.— 
Hartmann & Chagas, 1910, 164.— Herrick, W. W., 1910, 664, 665.— Hoppe- 
Sf-yler, 1904 a, 647.— Hoyt, 1908, 26; 1908, 417.— Huber, 1909, 265.— 
von Janicki, 1909, 386, 392 (bystolitica).— Jelks, 1910, 128-131; 1910, 
202-205; 1910, 94-97 (bystolitica).— Juergens, 1903, 841; 1907, 771-781, 
782, 784, 787, 789, 797, 801, 815.— Kaestner, 1906, 11.— Kartulis, 1906, 354, 
356-382, figs, a-1.— Kiewiet de Jonge, 1904 a, 79, 81, 89, 91.— King, 1911, 
L83, 184, 185, 186, 187.— Kisskalt & Hartmann, 1907, 112, figs. 5, 6; 1910, 
27, 2'.). fi^s. 12, 13.— Koidzumi, 1909, 650, 651.— Kuenen, 1909, 549, 550, 
551, 563 (hystolitica).— Leishman, 1906, 610.— Lesage, 1904 a, 1237, 1239; 
1905 a, 11, 16; 1908, 110, figs. 12-16; 1908, 585.— Liston, 1911, 108, 117.— 


Entamoeba — Continued. 

histolytica — Continued. 
Loewenthal, 1903, 2G7.— Luehe, 190G, 73; 1909, 421.— McCarriecm, 1909, 

735, 736.— Manson, 1907, 437, 440, 444.— Marshall, I). G., 1912, lux, 109— 
Martin, C. F., 1911, 645; 1911, 126.— Mathis & Leger, 1911, 208.— Max- 
well, J. P., 1909, 248.— Menetrier ft Tauraine, 1008, 909— Mercler, 1910, 

144. 147.— Messineo, 1911, 242 (hystolitica ) .— Metcalf, 1910, 315 Meyer, 
1906, 1327, 1328.— Minchin, 1907, 17, 18; 1909, 17, 18.— Musgrave ft Olegg, 
1906, 911, 915, 916, 917, 922, 929, 935, 938, 939, 941. 946, 947.— Noc, 
1909, 178, 179, ISO, 185, 186, 188, L89, 190, 191, 202.— de Oliveira, 1904 b, 
331; 1905, 200.— Popoflf, 1911, 210, 211.— von Prowazek, 1904 1, 43, 44; 

1911, 346; 1912, 30; 1912, 273; 1912, 242, 246.— Rosenberger, 1911, 30.— 
Ruge, 1903 q, 571; 1906 b, 4, 5, 6, figs. 2, 3.— Saundby & Miller, 1909, 
771-773.— Schepotieff, 1910, 495, 497, 498.— Scbubotz, 1905 b, 5. 6, 17 
(hystolitica).— Simon, C. E., 1907, 286; 1911, 213.— Simon, S. K., 1909, 
1528; 1910, 194.— Sistrunk, 1911, 1507, 1509.— Sluiter & Swellengrebel, 

1912, 22, 23, 24, 25, 26, 27, 164, figs. 8 a-b, 9.— Smith, A. J., 1911, 31.— 
Smith, A. J., & Weidman, 1910, 295, 296, 297.— Stiles, 1905 e, 297, 298, 
301-303; 1907 e, 525, 526; 1911, 1276; 1911, 1348.— Stitt, 1910, 190, 193, 
303.— Strong, R. P., 1907 a, 497, 500.— Tanaka, 1910, 2300 ( histologics ).— 
Tayler- Jones, 1904, 13, 14.— Vedder, 1907 a, 190, 191, 192.— Verdun, 1905 a, 
58; 1907 a> 30 (bystolitica).— Viereck, 1906 e, 1064, 1066; 1907 c, 9, 12, 
13, 14, 19, 28, 29, 33.— Vincent, 1908, 914; 1909 a, 78, 79.— Vollbracbt, 
1904 b, 163, 164.— Walker, 1908 a, 381, 383, 404, 406, 413, 423, 431, 433, 
435, 439, 440, 449; 1911, 260, 261, 262, 263, 264, 271, 273, 274, 275, 276, 
pi. 4, fig. 12, pi. 5, figs. 14, 15, 16.— Wallace, 1912, 689, 691, 692.— Wells, 

1911, 205, 206, 207.— Wenyon, 1908 b, 128, 129; 1908 k, 1245.— Werner, 
1908 e, 425, 430 (7, 12), figs. 16-35; 1909, 588; 1909, 241, 242, 243, 244, 
figs. 16-35; 1911, 75.— White, 1911, 112 (histolitica).— Whitmore, 1911, 71, 
72, 73, 75, 76, 79; 1911, 235; 1912, 515, 516, 517.— Williams, 1911, 267, 268, 
274, 275, 277, 278.— Williams & Gurley, 1910, 240, 241.— Wuelker, 1911, 
585, 594, 597, 609.— Young, W. B„ 1910, 586 (hystolytica). 

histolytica dysenterke Hara, 1910, 340, 367. 

histolytica var. tetfaffina Walker, 1911, 279, pi. 5, fig. 13. 

hominis Casagrandi & Barbagallo, 1897, 163— Albu, 1905, 435.— Barbagallo, 
1905, 73-75; 1905, 282; 1905, 145, 146; 1906, 380, 381.— Castellani & 
Chalmers, 1910, 220.— Fantham, 1911, 113, 116, 118.— Guiart, 1910, 142.— 
Kuenen, 1909, 549, 550, 551, 564.— Prues, 1905, 30.— Schaudinn, 1903 a, 
564.— Stiles, 1905 e, 296.— Verdun, 1904 f, 388; 1907 a, 29.— Viereck, 1907 c, 
29.— Walker, 1908 a, 432, 440, 449.— Werner, 1911, 67. 

intcstinalis (Walker, 1908).— Doflein, 1909, 508; 1911, 585.— Fiebiger, 1912, 
76.— Smith, A. J.. & Weidman, 1910, 296. 

kartuUsi (Doflein, 1901).— Castellani & Chalmers, 1910, 214.— Craig, 1911, 
36,* 234, 235.— Doflein, 1909, 506; 1911, 593.— Sluiter & Swellengrebel, 

1912, 26.— Smith. A. J., & Weidman, 1910, 295, 297. 
loeschi Lesage, 190S, 105; 1908, 584, 585. 
ma.viUaris Kartulis, 1906, 356. 

meleagridis (Smith, 1895).— Doflein, 1909, 508; 1911, 585.— Fiebiger, 1912, 
76.— Smith, A. J., & Weidman, 1910, 296. 

minuta Elmassian, 1909, 335-351, figs. 1-53.— Chatton, 1910, 287, 288, fig. 
5 n-p.— Chatton & Lalung-Bonnaire, 1912, 139.— Craig, 1911, 10, 36, 73. 
200-207, fig. 27; 1912, 3; 1912, 4.— Doflein, 1911, 577.— Fantham, 1911, 
115, 116, 118.— Glaeser, 1912, 103.— Hartmann, 1911, 51; 1912, 176.— 
Hartmann & Whitmore, 1912, 187.— Liston, 1911, 108.— von Prowazek, 


Entamoeba — Continued . 

minuta — Continued. 

1912, 244.— Sluiter & Swellengrebel, 1912, 23.— Walker, 1911, 262, 271 — 
Wuelker, 1911, 597. 

miurai (Ijirna, 1898).— Castellani & Chalmers, 1910, 214.— Craig, 1911, 234- 
235.— Sluiter & Swellengrebel, 1912, 27. 

mortinataUum Smith, A. J., & Weidman, 1910, 285-298, figs. 1-19; 1910, 
359-360 ( mortinatalitum ) . 

morula Raff, 1912, 346-351, figs. 1, 2, pi. 71, figs. 1-9. 

muris (Grassi, 1882 ) .— Alexeieff, 1912, 65.— Braun & Luehe, 1909, 19; 1910, 
20, 22.— Calkins, 1908, 423, 424; 1909, 141, 142, fig. 59.— Castellani & 
Chalmers, 1910, 215.— Chatton, 1910, 284, 287, 288, 325, fig. 5 v-y.— Chatton 
& Lalung-Bonnaire, 1912, 142.— Craig, 1912, 4.— Dobell, 1908, 432; 1909, 
246, 253, 259.— Doflein, 1907, 269, 279 ; 1909, 496-497 ; fig. 436 ; 1911, 595, 
figs. 525, 526.— Glaeser, 1912, 30, 74, 90, 104, 113, 118.— Hartmann, 1907, 
143; Hartmann in Hartmann & Naegler, 1908, 113; Hartmann, 1908, 
122 [222] ; 1909, 209 ; 1910, 8, 9.— Hartmann & Chagas, 1910, 164.— Hart- 
mann & Whitmore, 1912, 186, 189.— Kisskalt & Hartmann, 1910, 26, fig. 
8.— Luehe, 1909, 421.— McCarrison, 1909, 732, 733, 731.— Mercier, 1910, 
167.— Naegler, 1909, 5.— Popoff, 1911, 210.— Smith, A. J., & Weidman, 

1910, 296.— Walker, 1911, 268.— Whitmore, 1912, 517.— Wuelker, 1911, 594. 
nipponensis Doflein, 1911, 579. 

nipponica Koidzumi, 1909, 650-654, figs. 1-7. — Alexeieff, J 1912, 105. — Bu- 
chanan, R. E., 1911, 416.— Craig, 1911, 10, 36, 73, 207-212 ; 1912, 3 ; 1912, 
4.— Fantham, 1911, 115, 116, 118.— Greig & Wells, 1911, 8.— Hara, 1910, 
340 (nipponika).— Hartmann, 1911, 51, 55, 57; 1912, 165, 175.— Sluiter & 
Swellengrebel, 1912, 23.— Walker, 1911, 262, 269, 275.— Whitmore, 1911, 
75, 76 ; 1912, 517.— Wuelker, 1911, 597. 

nuttalli Castellani, 1908, 101-102, pi. 8.— Chatton, 1912, 180 (nuttali).— 
Craig, 1912, 4 (nutalli).— Walker, 1911, 268 (nutalli). 

ondulans Billet, 1907, 217. 

paedophthora (Caullery, 1906). — Castellani & Chalmers, 1910, 215. 

phagocytoides Guaducheau, 1907, 486-487, figs. 1-4; 1908, 493-494.— Castel- 
lani & Chalmers, 1910, 222, 232, 925, 976.— Craig, 1911, 36, 73, 213-214.— 
Fantham, 1911, 114-115, 116, 119.— Gauducheau, 1911, 172-173.— Walker, 

1911, 263. 

pitheci von Prowazek, 1912, 246-247. 

polecJci von Prowazek, 1912, 274, figs. 1-6. — Craig, 1912, 4. — von Prowazek, 

1912, 30; 1912, 244. 

!>ulmonalis (Artault, 1898).— Castellani & Chalmers, 1910, 214.— Craig, 

1911, 235.— Sluiter & Swellengrebel, 1912, 26. 
ranae Hartmann, 1907, 143.— Dobell, 1909, 245. 

ranarum (Grassi, 1879). — Alexeieff, 1912, 65. — Braun & Luehe, 1909, 19; 
1910, 20.— Castellani & Chalmers, 1910, 215 (ranorum).— Chatton, 1910, 
251; 1910, 283, 287, 288, 321, figs. 5 q-u, 6.— Chatton & Lalung-Bonnaire, 

1912, 142.— Craig, 1912, 4.— Dobell, 1908, 431, 432; 1909, 245-255, 257, pi. 
4, figs. 52-79 ; 1909, 711-721, figs. A-E.— Doflein, 1909, 497, 498, figs. 437, 
438; 1911, 596, 597, figs. 527, 528.— Erdmann, 1910, 341.— Glaeser, 1912, 
30, 74, 104, 113, 114, 118.— Hartmann in Hartmann & Naegler, 1908, 113 ; 
Hartmann, 1908, 122 [222] ; 1909, 209; 1910, 8, 9; 1912, 180.— Hartmann 
& Chagas, 1910, 164.— Hartmann & Whitmore, 1912, 185.— Mercier, 1910, 
144, 158.— Popoff, 1911, 210.— Walker, 1911, 268.— Whitmore, 1912, 516. 

schaudinni Lesage, 1908, 105, 108, 109 ; 1908, 584, 585, 586. 
sp. Fantham, 1911, 11&-114. 


Entamoeba — Continued . 

testudinis Hartmann, 1909, 209; 1910, 3-9, pi. 1, figs. 1-9.— Alexeieff, 1912, 
66; 1912, 97, 104-105.— Chatton, 1912, 111.— Craig, 1912, 4.— Doflein, 
1911, 598.— Glaeser, 1912, 113.— Hartmann, 1911, 16, fig. 4.— Hartmann & 
Cbagas, 1910, 102, 105; 1910, 165.— von Prowazek, 1911, 346.— Walker, 

1911, 268. 

tetragcna Viereck, 1907 c, 32.— Alexeieff, 1912, 105.— Ascoli, 1912, 393-394.— 
Bertarelli, 1912, 49, 50.— Braun & Luehe, 1909, 20; 1910, 21.— Brown, 
W. C, 1912, 223, 224, 225, figs. 3 A ; 3 B.— Bruinpt. 1910, 31.— Buchanan, 
R. E., 1911, 416, 422.— Castellani & Chalmers, 1910, 214-215, 221, 232, 
925, 976-977, 982.— Chatton, 1910, 260, 261; 1910, 268, 284, 286, 287, 
288, 289, 304, 310, 321, 322, fig. 5 1-m.— Chatton & Lalung-Bonnaire, 

1912, 139, 142.— Chlapowski, 1909, 87.— Craig, 1910, 5, 10; 1911, 6, 10, 

24, 25, 36, 60, 73, 89, 99, 143, 162, 163, 179, 179-200, 202, 205, 207, 208, 
209, 212, 217, 221, 228, 231, 233, figs. 22-25; 1911, 362-366; 1912, 1, 4, 
10, 15, 19, 20-25, 27, 80, 32, 33, pi. 2; 1912, 3, 4, 6, 11, 12, 13, 14.— Dobell, 
1909, 254; 1909, 314, fig. 24.— Dock, 1909, 85.— Doflein, 1909, 495, 496, 
figs. 434, 435; 1911, 22, fig. 19.— Dopter, 1910, 126.— Elmassian, 1909, 
335, 336, 337, 338, 340, 342, 343, 346.— Fantham, 1911, 114, 116, 117, 
118, 119.— Fiebiger, 1912, 75, fig. 14.— Franchini, 1911, 189-195, 1 fig., 
1 pi., figs. 1-2.— Gabbi, 1911, 136-138; 1911, 203; 1912, 587-58S.— Glaeser, 
1912, 98, 112, 113.— Hartmann in Hartmann & Naegler, 1908, 113; Hart- 
mann, 1908, 117-127 [217-227], figs. 1, 2; 1909, 209, 210, 211, 212, 213, 
216, 217, 218; 1910, 4, 5, 7, 8, 9 ; 1911, 6, 8, 15; 1911, 51, 52-58, 59, 61, 62, 
63, figs. 1-26, pi. 1, figs. 1-6; 1912, 163-181, figs. A-D, pis. 15, 16, figs. 
1-46.— Hartmann & Cbagas, 1910, 86, 101, 112; 1910, 165.— Hartmann & 
von Prowazek, 1907, 312 (tetragona). — Hartmann & Wbitmore, 1912, 
183, 184, 185, 188, 1S9, 190, 191, 192!— von Janicki, 1909, 384, 391, 392.— 
Kisskalt & Hartmann, 1910, 26-28, 29, figs. 9-11.— Koidzumi, 1909, 650, 
651.— Lesage, 1908, 105.— Liston, 1911, 108.— Luehe, 1909, 421.— Ma this & 
Leger, 1911, 208.— Mercier, 1910, 147.— Metcalf, 1910, 310, 315.— Naegler, 
1909, 40, 42; 1911, 68.— Noc, 1909, 187, 190, 201.— Noeller, 1912, 196, 197, 
199.— Popoff, 1911, 210.— von Prowazek, 1912, 245.— Schepotieff, 1910, 
495.— Sistrunk, 1911, 1507, 1509.— Sluiter & Swell engrebel, 1912, 22, 23, 

25, fig. 4.— Smith, A. J., & Weidman, 1910, 296.— Stiles, 1911, 1276.— 
Swellengrebel, 1910, 170. 171.— Takamiya, 1912, 5.— Tanaka. 1910, 2300.— 
Walker, 1911, 262, 263, 264, 271, 273, 276 (tetragina).— Wallace, 1912, 
689, 691.— Wells, 1911, 205, 207.— Werner, 190S e, figs. 1-15; 1909, 588, 
1909, 241, 242, 243, 244, figs. 1-15; 1911, 70, 75; 1912, 190-192.— Whit- 
more, 1911, 73, 75, 76, 77, 78, 79, fig. 1; 1911, 85; 1911, 235; 1912, 516^517, 
519.— W T Z5_ae58, 1911, 585, 594, 595, 597. 

tropicalis Lesage, 1908, 105, 108, 110, 111, figs. 7-11; 190S, 584, 585, 5S6.— 
Castellani & Chalmers, 1910, 214, 215, 219-220, 232, 347, 925.— Craig, 1911, 
10, 36, 73, 212-213; 1912, 3; 1912, 4.— Fantham, 1911, 112-113, 116, 117, 
118.— Kuenen, 1909, 552, 563.— Sluiter & Swellengrebel, 1912, 21.— Walker, 

1911, 263.— Whitniore, 1911, 72 ; 1911, 93. 

undulans Castellani, 1905, 67, 69.— Braun, 190S. 42.— Castellani, 1904, 50S; 
1905, 1286, fig. 2 b.— Castellani & Chalmers, 1910, 214-215, 220, 232, 
925.— Craig, 1911, 37, 73, 214-215.— Doflein, 1909. 50S ; 1911, 595.— 
Fantham, 1911, 115.— Minchin, 1907, 21; 1909, 21.— Sluiter & Swellengrebel, 

1912, 27.— Smith, A. J., & Weidman, 1910, 296.— Verdun, 1907 a, 32.— 
Walker, 1908 a, 423, 449; Walker, 1911, 261. 


Entamoeba — Continued. 

urogenitals (Baelz, 18S3).— Castellani & Chalmers, 1910, 214.— Craig, 1911, 
233.— Doflein. 1909, 505; 1911, 593.— Sluiter & Swellengrebel, 1912, 26.— 
Smith, A. J.. & Weidman, 1910, 296. 

williamsi von Prowazek, 1911, 349, pi. 17, figs. 1-5. — Alexeieff, 1912, 70. — 
Craig, 1912, 4.— Hartmann & Whitmore, 1912, 185, 187, 189, 192.— von 
Prowazek. 1912, 30 : 1912, 273 ; 1912, 242, 244, 245. 
Loeschia Chatton & Lalung-Bonnaire, 1912, 142.— Alexeieff, 1912, 149.— Chatton, 
1912, 111. 

braziliensis Chatton, 1912, 182. 

coli (Loesch, 1875).— Chatton, 1912, 181, 182; 1912, 110, 111. 

histolytica (Schaudinn, 1903). — Chatton & Lalung-Bonnaire, 1912, pi. 9, 
fig. 14. 

minuta (Elmassian, 1909).— Chatton, 1912, 182. 

sp. Chatton, 1912, 1S0-182, pi. 10, figs. 1-5. 

tetragena (Viereck. 1907).— Chatton, 1912, 181, 182; 1912, 109.— Chatton & 
Lalung-Bonnaire, 1912, pi. 9, fig. 14. 
Paramoeba Schaudinn, 1896 b, 31^1.— Braun, 1908, 42.— Calkins, 1901 b, 59, 93, 
105, 218, 233, 234, 276.— Castellani & Chalmers, 1910, 214, 223.— Craig, 
1911, 12, 23, 29, 36, 215.— Doflein, 1909, 510-512.— Gedoelst, 1911, 33.— 
Guiart, 1910, 156.— Hartmann & von Prowazek, 1907, 311, 313, 315, 320.— 
Sluiter & Swellengrebel, 1912, 27. 

coli (Loesch, 1875).— Doflein, 1911, 1031 (index). 

eilhardi Schaudinn. 1896 b, 31-41, figs. 1-12.— Castellani & Chalmers, 1910, 
223.— Craig, 1911, 29, 216, 219, 222.— Dobell, 1909, 312, fig. 21.— Doflein, 
1907, 281; 1909, 26. 152, 180, 511, figs. 155, 452; 1911, 164, 602, figs. 172, 
532.— Glaeser, 1912, 53, 97, 105, 122.— Hartmann & von Prowazek, 1907, 
311, 320, 328.— Moroff, 1908, 200.— Schubotz, 1905 b, 4. 

hominis Craig, 1906, 214-220, figs. 1-2.— Braun, 1908, 43.— Castellani & 
Chalmers, 1910, 223, 232, 925.— Craig, 1910, 1-11, figs. 1-2; 1911, 10, 29, 
36, 73, 132, 215-229, figs. 28-29.— Doflein, 1909, 512, fig. 453 ; 1911, 603.— 
Gedoelst, 1911. 34, fig. 34.— Hickson, 1909, 83.— Schepotieff, 1910, 499 — 
Simon, C. E.. 1907, 289; 1911, 216.— Sluiter & Swellengrebel, 1912, 27 — 
Thornburgh, 190S, 56.— Walker, 1911, 261-262. 
Poneramoeba Luehe, 1909, 421. 

histolytica (Schaudinn, 1903).— Luehe, 1909, 418^24. 
Proctamoeba Alexeieff, 3 912. 55-74. 

maris Alexeieff. 1912. fig. 5 (1 & 2). 

ranarum Alexeieff, 1912, 66, figs. 6, 7. 

salpae Alexeieff, 1912, 64, fig. 5 (3-5). 
Vahlkampfia Chatton & Lalung-Bonnaire, 1912, 135-142.— Alexeieff, 1912, 149, 
150.— Chatton, 1912, 110, 111, 112, 113. 

hartmanni (von Prowazek, 1912). — Chatton, 1912, 112. 

lacertae (Hartmann & von Prowazek, 1907). — Chatton, 1912, 112. 

Umax Alexeieff, 1912, 150, 151. 

mucicoln (Chatton. 1909).— Chatton, 1912, 112. 

poedophtora (Caullery, 1906).— Chatton, 1912, 112. 
Viereckia Chatton & Lalung-Bonnaire, 1912, 142. 

tetragena (Viereck, 1907).— Chatton, 1912, 110. 



By Dr. Gary N. Calkins, Professor of Protozoology, Columbia University, New 

York City. 

" Die Kenntniss der Entwickelung ist das erste Postulat der Pro- 
tozoenforschung. Schaudinn 1903." 

The above quotation should be made an axiom and incorporated in 
every taxonomic paper on protozoa, especially on rhizopods. Until 
the full life history is known we can only place forms provisionally 
and with the understanding that further research alone will establish 

The taxonomic problems of the amoebae were not particulary dif- 
ficult to handle until the pathogenic forms became known and arti- 
ficial culture methods were developed. Then the difficulties were to 
determine between pathogenic and inocuous forms. Free living 
small amoebae may be cultivated with ease on artificial culture media, 
pathogenic forms less easily, and the problem of distinguishing be- 
tween them soon began to give trouble. It is claimed by many that 
small forms of free living rhizopods may become encysted, and 
within the protection of their cysts withstand the digestive fluids 
of their vertebrate hosts, with or without emerging from their 
coverings. This led, furthermore, to the claim that all or a 
large proportion of the cultivated amoebae, paid to be pathogenic or 
parasitic, were in reality only encysted stages of free living rhizo- 
pods. Within the last few years, therefore, there has been developed 
a great interest in the systematic positions of amoebae that will live 
on artificial culture media. The chief source of the confusion that 
has arisen is the group of minute water or infusion amoebae and not 
the relatively large free living forms like Amoeba proteus, A. ves- 
pertilio, and their allies. Some of the smaller ones are sufficiently 
characteristic to be easily identified. A. verrucosa, for example, with 
its corrugated surface, is not easily mistaken for other forms. It is 
different, however, with that group of minute forms usually included 
under the specific name Amoeba Umax Dujardin. 

At the present time it is recognized that the nature of the pseudo- 
podia and ectoplasmic and endoplasmic differentiation are unsafe 
diagnostic characters by which to identify amoebae, for these have 
been shown to vary widely in the same species under different condi- 
tions of environment. Nuclear differences, however, appear to be 
more stable, and we find a growing tendency, mainly emphasized by 
Nagler, Chatton, and Glaser, to base specific differences on the 
changes which the nuclei undergo during division. 

The enormous differences between amoeboid types of rhizopods not 
only justifies but makes imperative generic separation amongst them. 
The characteristics of A. proteus are definite and distinct, but the 


characterization of a genus of which A. proteus is the type species 
would hardly suffice to characterize the widely divergent types that 
have been discovered in recent years. This conclusion has been in- 
dependently reached by all students of the rhizopods, some of the re- 
sults being seen in the genera Paramoeba and Entamoeba now well 

The life history of Amoeba proteus, as well as the morphological 
features, is sufficient to separate it from the other and smaller free 
living forms that lend themselves to the agar culture method. The 
latter, belonging for the most part to the so-called " limax " group, 
have been extremely difficult to deal with systematically. Dujardin 
in 1841 created the species as a type of amoeba, but his description 
was so indefinite that no one at the present time can be sure of the 
form meant by this gifted pioneer. Penard in 1902 likewise gave an 
inadequate description, and many modern investigators, working 
with forms which they call Amoeba Umax, have come to opposite 
conclusions regarding structures and activities, and much confusion 
has resulted. Vahlkampf in 1904 gave a careful description of a 
small form measuring about 3|x which he designated A. Umax. The 
various phases of activity, including encystment, emergence from the 
cyst, and the details of nuclear division, were carefully made out. If 
we were to retain the name "limax," therefore, it would have to 
be based upon the characters described by Vahlkampf. 

While retaining the specific name limax of Dujardin for Vahl- 
kampf 's species we agree with Chatton 1912 in giving it a different 
generic name from that of Amoeba proteus and accept Chatton's 
term Vahlkampfia as a generic name for part of the forms included 
formerly under the name Amoeba. We do not agree with Chatton, 
however, in abandoning the old name limax, but would retain it for 
the species Vahlkampfia limax Duj. emend Vahlk. Not only are 
forms included under the new genus Vahlkampfia different from 
Amoeba proteus but they also differ from other types of minute 
amoebae formerly included as limax forms. Here, for example, are 
those species which, on agar, pass from a pseudopodia bearing stage 
to a flagellum bearing stage, and vice versa. For these we have 
adopted Alexeieff's name Nagleria, but with emendations, however, 
since Alexeieff included under this name all of the forms herein 
grouped under the name Vahlkampfia. 

The views expressed in the preceding paragraphs may be sum- 
marized in the statement that the old genus Amoeba should be broken 
up into allied genera as follows: Amoeba, Vahlkampfia, Nagleria, 
Craigia, Trimastigamoeba, Entamoeba, and Paramoeba. 

Note. — No attempt has been made to make the bibliographies complete; the 
number of titles that might be added is legion, and no donbt many able works 
on the amoebae bave been omitted. These can be obtained from the references 



Behla, R. 1897. Die Amoben, insbesondere vom parasitiiren uud Kulturellen 

Standpunkte. Berlin. 
Cash and Hopkinson. 1905. The British Freshwater Rhizopods and Ileliozoa 

Ray Society. London. 
Craig, C. F. 1912. The Parasitic Amoebae of Man. 
Doflein, F. 1911. Lehrbnch der Protozoenkunde. Jena. 
Pcnard, E. 1890. Etudes sur les rhizopodes d'eau donee. Mem. de la Soc. 

de Phys. et de l'histoire nat. de Geneve. Tome 31. 
Penard, E. 1902. Faune rhizopodique du bassin du Leman. Geneve. 
Wiilkr, G. 1911. Die Tecknik der Amoebenzuchtung. Cent. f. Bakt. Nos. 

19, 21. 

Genus Amoeba, Bory. 

Eosel von Rosenhof in 1755 described a small organism under the 
name of " der kleine Proteus." The value of his description was 
recognized by Linnaeus, who gave to the organism the name Volvox 
chaos. Pallas also distinguished it under the name of Volvox 
proteus, while Bory de Saint Vincent in 1824 gave to it the generic 
name Amiba, which Ehrenberg in 1831 changed to its modern form 
Amoeba. Many recent writers have discarded the "o" and spell it 
Ameba, but their only justification would be to return to the original 
form and spell it Amiba. 

The type form of the genus is A. proteus of to-day, which corre- 
sponds with Ehrenberg's A. princeps and with Rosel's kleine Proteus. 

Generic characters. — Free living rhizopods, usually of large size 
(up to 1 mm. in diameter), with one or many nuclei and one or more 
contractile vacuoles. The protoplasm is differentiated into ectoplasm 
and endoplasm, pseudopodia forming from both parts or only from 
ectoplasm. The nuclei are large, with thick doubly refracting mem- 
branes and with chromatin concentrated in a single large karyosome 
or in granular form distributed throughout the nucleus. Reproduc- 
tion by division and sporulation. 

Amoeba proteus Pallas. 
Synonyms : 

Der kleine Proteus, Rosel von Rosenhof, 1755. 

Volvox proteus, Pallas, 1766. 

Amiba divergens, Bory de St. Vincent, 1822. 

Amoeba princeps, Ehrenberg, 1831, 1838. 

Amoeba proteus, Leidy, 1878, 1879. 

Amoeba radiosa, Ehrenberg, 1830, 1831, 1838. 
Leidy, J. 1878. Proc. Ac. Nat. Sc, Philadelphia. 

Leidy, J. 1S79. Fresh Water Rhizopods of North America, Washington. 
Awerinzeff, S. 1904. Ueber die Theiluug bei Amoeba proteus. Zool. Ana. 

Bd. 27. 
Calkins, G. N. 1907. The Fertilization of Amoeba proteus. Biol. Bull., vol. 13 
Metcalf, M. M. 1910. Studies on Amoebae. Jour. Exper. Zool., vol 9, No. 2. 

00692— vol 2, pt 1—13 19 


Prandtl, H. 1907. Die physiologische Degeneration der Amoeba proteus. 

Arch. f. Prot. Bd. 8. 
Scheel, R. 1899. Beitrage zur Fortpflanzung der Amoben. Festchr. von K. v. 

Kupffer, Jena. , ^ 

Schubotz. 1905. Beitrage zur Kenntnis der Amoeba blattae u. A. proteus. 

Arch. f. Prot., vol. 6. 

Large fresh-water form from 300-600pi. The ectoplasm is clearly 
defined, the endoplasm granular and vacuolated and takes part in the 
formation of the lobose pseudopodia. The nucleus in vegetative 
stages is single and has a thick membrane, chromatin usually in the 
form of granules. The contractile vacuole is large and definite, open- 
ing to the outside at the posterior end of the organism in motion. 
Keproduction by division and sporulation. Gametogeny preceded by 
the multiplication of nuclei, formation of secondary conjugating 
nuclei and development of secondary reproductive cysts (Calkins). 
The swarmers are amoeboid (Scheel) . Young cells with stellate form 
formerly known as A. radiosa. Food, small animals, algae, diatoms, 
other protozoa, etc. Not viable on protozoan agar or other media. 
Common in fresh-water ponds and ditches among dead leaves and 
other detritis. 

Note. — The process of gametogeny as described by Calkins has been criti- 
cized by Prandtl, Schubotz, Dobell, and others on the ground that the struc- 
tures described were stages in the development of parasites. Scheel and Met- 
calf have confirmed my observations in part, but have not seen the identity, 
possibly because of the poor figures in my original paper. After careful com- 
parison of amoebae parasitized by Nucleophaga and by the form described by 
Prandtl under the name "Allogroniia," I find no reason whatsoever for chang- 
ing my views regarding autogamy as originally described. 

A. vespertilio Penard. 

Penard, E. 1902. Faune rhizopodique du Bassin du Leman. Geneve. 
Doflein, F. 1907. Studien zur Naturgeschichte der Protozoen. V. Amoben- 
studien. Arch. f. Prot. Suppl. 1, 1907. 

Common fresh- water form from 200-300[jl. In motion the pseudo- 
podia are usually pointed and triangular in outline; at rest they 
are radially arranged and often very long and thin. The nucleus is 
spherical, containing a globular karyosome in which the bulk of the 
chromatin is massed, and a peripheral substance containing little 
chromatin. Reproduction by fission in rounded forms in which the 
long pseudopodia are replaced by small papilliform processes. The 
karyosome divides by "mitosis;" a cell division following after a 
longer or shorter time. The resting cysts are globular with a thin 
gelatinous membrane. Multiple agamous reproduction sometimes 
occurs within the cysts in which the nucleus divides three times, re- 
sulting in the formation of eight young amoeboid forms. Sexual 
processes not known. Habitat pools and ponds similar to that of A. 
proteus. Not viable. 


A. flava Greeff. 

Greeff, B. 1891. Ueber die Erdamoben. Sitz. Ber. d. Ges. zu Bef. de Ges. Wisa 

zu Marburg. 
M<ibius, K. 1888. Bruckstiicke einer Rhizopodenfaune der Kieler Bucht. Abb. 

d. Berlin Akad. Wiss. Bd. 49. 
Schepotieff, A. 1910. Amobenstudien, Zool. Jahrb. ADat. Bd. 29, p. 485. 

Large salt-water amoeba up to 1 mm. in length; young forms uni- 
nucleate ; old forms multinucleate. The pseudopodia of young forms 
are short and radial in arrangement; protoplasm finely granular with 
peripheral ectoplasm and brownish-colored endoplasm, the latter 
taking no part in pseudopodia formation. Pellicle absent. The 
single nucleus has a doubly-refracting membrane, chromatin in the 
form of fine granules and with a central karyosome. This is the type 
studied by Greeff, by Gruber, and by Mobius. The nucleus divides 
by mesomitosis with the formation of nuclear plate at times; details 
not known. 

The small uninucleate form grows and the nuclei divide until in the 
large forms they number from 45-80. These then fragment to form 
chromidia and the cell encysts. The cysts are oval or spherical from 
500-525(jl in diameter and of brownish -black color. The cyst wall is 
opaque and consists of two layers — an outer layer rough and warty, 
and an inner smooth layer. The chromidia form secondary nuclei 
which become the nuclei of isogametes with one flagellum. These con- 
jugate two by two (not actually observed), and the result of con- 
jugation is the formation of a uninucleate copula or zygote which 
transforms into a young uninucleate amoeba (Schepotieff). Habitat, 
salt water, Naples. 

A. verrucosa Ebr. 
Synonyms : 

Amoeba terricola, Leidy. 
Amoeba striata, Leidy. 
Amoeba sphaeronucleolus, Greeff. 
Ehrenberg, C. G. 1838. Die Infusionsthierschen als volkommne Organismen. 

Gliiser, H. 1912. Untersuchungen liber die Theilung einiger Amoben. Arch. 

f. Prot. Bd. 25, p. 27. 
Rhumbler, L. 1898. Pbysik. Analyse von Lebonsersoheinungen der Zelie. 
Arch. f. Entwickl. Vol. 7, p. 103. 

Fresh- water form much smaller than A. proteus, 80— IOO^l. It is a 
sluggish form with dense ectoplasm and a still denser pellicle. Its 
protoplasm is yellowish to white and transparent. Pseudopodia are 
few in number, forming a lamella-like process at one end. The 
pellicle is thrown into folds giving the characteristic striated ap- 
pearance thus distinguishing it from other free living amoebae. The 
nucleus is relatively large, oval, or spherical in form, with a con- 
spicuous karyosome and an ex-centric nucleolus. A single contractile 
vacuole is invariably present but t lie- endoplasm has few vacuoles., 


Nuclear division promitotic with pole bodies and central nuclear 
plate (Glaser). Reproduction by division the only known method of 
increase. This species is very close to if not identical with A. ter- 
ricola. Green . 


A. terricola, Greeff. 

Similar to, if not identical with Amoeba verrucosa, Ehr. 

Greeff, R. 1891. Ueber die Erd-Anioeben. Sitz. Ber. d. Ges. d. Naturwiss. 

zu Marburg. 
Leidy, J. 1879. The Fresh Water Rhizopods of North America. Washington. 
Cash and Hopkinson. See No. 2. 
Grosse-Allermann, W. 1909. Studien iiber Amoeba terricola. Arch. y f. Prot 

V. 17. 

Sluggish form from 90-200[a similar in general characters to A. 
verrucosa. Its rhizopod characters are said to be difficult to de- 
termine owing to its slow movements and crystalline appearance. 
The pseudopodia are slow to form, very blunt and short. The ecto- 
plasm and endoplasm are distinct, but the former is only a small 
zone about the cell which is bounded by a definite pellicle. The endo- 
plasm is alveolar witl^ large refringent granules or crystals. Nuclei 
are one or many in number and contractile vacuoles are numerous. 
The nuclei vary in size from 20— 30p. with large and distinct karyo- 
somes. Reproduction by fission and possibly by multiple division, 
but details are unknown. (See Gross- Allermann. ) Habitat, moss. 
-In addition to these well-known amoebae there are others of allied 
t}^pe belonging to the genus Pelomyxa. These are large forms with 
many nuclei and with very sluggish movement without definite 
pseudopodia formation. Schaudinn's Amoeba binucleata is some- 
times placed here. 

Genus Vahlkampfia Chatton, emend Calkins. 

Synonyms : 

Nagleria (in part) Alexeieff. 
Hartmannia (in part) Chatton. 

Alexeieff, A. 1912. Sur les caracteres cytologiques et la systematique des 
Amibes du groupe limax (Nagleria nov. gen. et Hartmannia nov. gen.), etc. 
Bull, de la Soc. Zool. de France, vol. 37, No. 2. 

Chatton, E. 1912. Sur quelques genres d'amibes libres et parasites. Synony- 
mies, homonomie, Impropriete. Bull. d. la. Soc. Zool. de France, vol. 37, No. 3. 

Chatton and Lalung-Bonnaire 1911. Amibe limax (Vahlkampfia nov. gen.) dans 
l'intestin humain. Bull, de la Soc. de Path Exot., vol. 5, p. 135. 

For reasons given in the introduction we follow Chatton in plac- 
ing some of the forms belonging to the " limax " group and included 
^ronerally in the old genus Amoeba, in a new genus named after Vahl- 
kampf who first accurately described one of this miscellaneous col- 
lection. We find it necessary, however, to limit the genus somewhat 
more narrowly than does Chatton, by eliminating those types with 
the capacity to change from amoeboid into flagellated forms and 


vice versa. These types we place in AlexeiefTs genus Nagleria char- 
acterizing the genus Vahlkampfia as follows : 

Minute free-living or commensal rhizopods moving as a finger- 
formed single pseudopodium or with irregular ectoplasmic outbursts 
to form a local or general hyaline ectoplasm. The nucleus is single 
or double with finely divided chromatin forming a membrane-like 
contour and with a definite karyosome. Reproduction by simple 
division, the karyosome dividing first like the nucleolus-centrosome 
of Euglena, the peripheral chromatin forming the nuclear plate 
(promitosis of Niigler). Cysts uninucleate. Food bacteria; habitat 
usually fresh water in ponds, etc., but many types are found in 
garden earth and some may be marine. 

Vahlkampfia Umax Duj. emend Vahlkampf. 
Synonyms : 

Amoeba Umax Dnjardin. 
Amoeba Umax of authors in part. 
Alexeieff, A. 1912. See preceding bibliography. 
Chatton, E. 1910. Essai sur la structure du Noyau et la mitose chez les 

Amoebiens. Arch. d. Exper. et Gen. Tome 5. No. 6. 
Dujardin, F. 1841. Les Infusoires in Suites de Buffon. Historie naturelle 
des zoophytes. 

Minute form from 3— 4pL in length and 0.75^ in width. Movement 
in a zigzag manner by the formation of pseudopodia first on one side, 
then on another in the general direction of movement. The anterior 
end during movement is broader than the posterior end. There is no 
differentiation into ectoplasm and endoplasm, except Avhere the 
pseudopodia are forming. One contractile vacuole is present in the 
posterior part of the cell and is distinctly visible. The nucleus is 
single, visible in the living cell, and from 0.3-0.5[j. in diameter. 
When stained the nucleus shows a membrane lined by chromatin, a 
colorless zone within the membrane and a distinct spherical karyo- 
some in the center. At division this karyosome first elongates then 
constricts in the middle and divides, the nuclear plate being formed 
from the peripheral chromatin. •The colorless zone forms an elon- 
gated matrix in which indistinct fibers ultimately appear. The 
daughter plate chromatin collects in a mass on one side of the daugh- 
ter karyosome and then breaks up to form the peripheral layer 
around the membrane. The cysts are spherical, uninucleate and 
about 1.5pi in diameter. The cyst wall is brown in color but trans- 
parent. Contractile vacuole absent. Viable. 

Vahlkampfia paedophthora Canllery. 
Synonym : Amoeba paedophthora Caullery. 

Caullery, M. 1910. Sur un amoebien parasite des embryons de Peltogaster 
curvatus Koss. C. R. Soc. Biol, de Paris Tome 61. 

Small form parasitic in the eggs of Peltogaster a crustacean. En- 
doplasm highly vacuolated, nucleus minute with distinct karyosome. 


Division promitotic. Said to be an active agent in the destruction of 
eggs and embryos of the crab. 

V. froschi Hartmann. 

Synonym : Amoeba froschi Hartmann. 

Hartmann und Prowazek, 1907. Blepharoplast, Karyosom, und Centrosom. 

Arch. f. Prot. Bd. 10. 
Glaser, H. 1912. See bibliography, p. — . 
Nagler, K. 1909. Entwicklungsgeschichtliche Studien fiber Amoben. Arch. f. 

Prot. Bd. 15, p. 1. 

Small forms usually from 8— 12jx in diameter. Nucleus from 1-2jjl 
Movements similar to those of V. Umax. The nucleus is central with- 
out a firm membrane and with a distinct karyosome and centriole. 
Glaser interprets the latter as only a part of the karyosome which 
retains the stain longest and does not regard it as a definite body. 
Its independent division, however, seems to show that it is quite as 
independent as the centrosome of higher cells. Nuclear division is 
slightly different from that of V. Umax by reason of the concen- 
tration of chromatin in the karyosome. Nuclear plate, polar masses, 
and reconstruction are similar to those of limax, the division there- 
fore is promitotic. The cysts are spherical, from 7-lOpi and with 
double membrane. Sexual processes said to be autogamous (Nagler). 

V. lacustris Nagler. 

Synonym : Amoeba lacustris Nagler. 

Nagler, K. 1909. See preceding bibliography. 

Minute forms, from 8-15 jjl with only slight differences from other 
limax forms. The small peculiarity of the nuclear plate in division 
does not seem to us a sufficient characteristic for a distinct species, 
and until its life history is made out this form should be considered 
only a variant of V. limax. The cyst is uninucleate, transparent, 
and without marked characteristics. Fresh water. 

V. lacertae Hartmann. 

Synonym : Entamoeba lacertae Hartmann, 1907. 

Hartmann und Prowazek, 1907 

Nagler, K. 1909. See above. 


Small form, from 10-20 \l in diameter, with highly vacuolated cyto- 
plasm and distinctly visible nucleus. The karyosome is surrounded 
by a peripheral row of chromatin granules which fuse to form larger 
masses bound together by a fine reticulum. A centriole is plainly 
seen even in the living state. Nuclear division is promitotic. The 
cysts are smaller than the vegetative forms and have no marked 
characteristics beyond a slightly wrinkled outer membrane. Habitat, 
commensal in the gut contents and cloaca of lizards. Viable. 

V. albida Niigler. 

Synonym: imoeba albida N&gler. 

Nagler, K., 1909. Entw. Studien iiber Amoebeu. Arch. f. Prot. Bd., 15, p. 24. 

Larger form characterized by a hyaline or transparent cell body, 
slow movements, and distinct nuclear membrane, from 20-40 jx. Divi- 


sion of the nucleus promitotic. Sexual processes autogamic, with 
tetrad-like fertilization nuclei. Habitat, garden earth. Viable, 

V. horticola Nagler. 

Synonym: Amoeba horticola Xiigler. 

Nagler, K., 1909. See preceding bibliography. 

Small form, from 15-25 \l in diameter. Movement by protrusion 
of long pseudopodia; ectoplasm and endoplasm distinct, the latter 
with large granules and smaller refractive bodies and single con- 
tractile vacuole, difficult to see because of the granules. The nucleus, 
visible in the living cell, has a large karyosome surrounded by a 
hyaline zone. The division is promitotic, with centrioles. The chro- 
matin of the nuclear plate is said to differ from that of other Umax 
forms in being concentrated into six definite chromosomes. Cysts 
are 10 (jl in diameter, somewhat ellipsoidal in form. Sexual processes 
unknown. Habitat, garden earth. Viable. 

V. diploidea Hartmann and Nagler. 
Synonyms : 

Sappinia diploidea Alexeieff, 1912. 
Hartmannia Chatton, 1912. 
Hartmann u. Nagler, 1908. Kopulation bei Amoeba diploidea mit Selbstandig- 
bleiben der Gam^tenkerne wahrend des ganzen Lebenscyclus. . Sitz. Ber. d. 
Ges. Nat. Fr. Berlin, 1908. 

Small forms, from 15-30 ul in diameter; ectoplasm with distinct 
pellicle; nucleus double in the vegetative stages, each with karyosome 
and peripheral chromatin, and division is synchronous, promitotic in 
type. Conjugation occurs by fusion of two amoebae within a com- 
mon cyst, the two nuclei in each cell now uniting, the fused nuclei 
forming the two nuclei of the vegetative stages. Habitat, garden 
earth. Viable. 

V. mucicola Chatton. 

Chatton, E., 1909. Une Amibe, Amoeba mucicola n. sp., parasite des branchies 
des labres. C. R. Soc. Biol de Paris. Tome 67. 

Small forms, from 12-30 pi, with highly vacuolated endoplasm and 
limax-like ectoplasm. Nucleus visible as a clear vesicle, with a dis- 
tinct karyosome. Contractile vacuole not observed. Nuclear mem- 
brane limax-like. Division promitotic. Habitat, ectoparasitic on 
fish at Banyuls. 

V. polypodia Schultze. 

Synonym : Amoeba polypodia F. E. Schultze. 

Schultze, F. E., 1S75. Ithizopodenstudien, V. Arch. mik. Anat. Bd. 2. 

The identity of this amoeba is somewhat questionable and it has 
been accepted generally as a type which reproduces by direct division. 
Renewed study, however, with modern methods would probably show 
that it belongs to the limax type of promitosis, since Schultze de- 
scribed a hyaline zone around the highly refractive " nucleus " (kary- 
osome?). His observations were made solely on the living cell and 


the chromatin and nuclear plate were probably not seen. The ray- 
like pseudopodia, however, are characteristic. 

V. tachypodia Glaser. 
Synonym : Amoeba tachypodia Glaser. 

Glaser, H., 1912. Untersuchnngen liber die Theilung einiger Amoben. Arch, 
f. Prot Bd. 25. 

Small form, from 15-30 \l, which Glaser regards as a variety of 
Umax varying from the latter in ectoplasmic and nuclear structures. 
One contractile vacuole ; nucleus visible in life surrounded by a 
definite membrane and containing a hyaline zone, in the center of 
which is the karyosome. Movement rapid and form changes con- 
stant. Cysts from 10-11 jx, similar to those of limax. Nuclear 
division promitotie, the karyosome dividing by lateral constriction; 
nuclear plate with large chromatin granules. Habitat, pond or lake 
water. Viable. 

V. lamellipodia Glaser. 

Synonym : Amoeba lamellipodia Glaser. 

Glaser, H., 1912. See preceding bibliography. 

Larger forms, from 25-50 \l in length and 10-18 [x in width; ecto- 
plasm clearly defined about the entire cell, giving the impression of 

a lamella ; endoplasm highly vacuolated and filled with refractive 
granules; contractile vacuoles numerous. Nucleus distinct in life; 
no protective cysts in water. In agar cultures cysts sometimes ap- 
pear, easily recognizable by. the collection of deeply refractive gran- 
ules about the nucleus. Nuclear division is preceded by enlargement 
of the karyosome, which becomes vacuolated, while the zone about it 

becomes filled by a fine chromatic reticulum. The karyosome finally 
resolves into an achromatic spindle, with distinct chromosomes form- 
ing the nuclear plate. Pole bodies are absent^ division therefore 
mesomitotic. Habitat, pond water. Viable. 

T\ binucleata Gruber. 
Synonyms : 

Amoeba binucleata Gruber. 

Pelomyxa binucleata Doflein, 1911. 

Sappinia binucleata Alexeieff, 1912.- 
Gruber, 1884. Studien iiber Amoben. Zeit. wiss. Zool. Vol. 41, p. 208. 
Schaudinn, F., 1895. Ueber die Theilung von A. binucleata. Sit Ber. Ges. 
Nat Fr. Berlin. Bd. 6, p. 130. 

Larger form with double nuclei, which divide by synchronous meso- 

mitosis. Life history unknown, possibly a stage in the development 

of Pelomyxa, with which it is found. Habitat, pond water. 

V. guttula Dujardin. 
Synonyms : 

Amoeba guttula Dujardin, 1841. 

Amoeba platypodia Glaser, 1912. 
Dujardin, F., 1841. Histoire naturelle des zoophytes. Infusoires. 

Larger forms, from 30-50 |x, with highly transparent protoplasm; 
one contractile vacuole at the posterior end; ectoplasm distinct. 


Nucleus with great karyosome distinctly visible in life. Protective 
cysts absent. Nuclear division mesomitotic similar to that of A. 
lamellipodia, but the anaphase is characterized by the collection of 
chromatin into large polar masses resembling V. Umax. Habitat, 
pond water. Viable. 

This is the same species evidently as the one described by Gliiser 
under the name A. platypodia, which is somewhat smaller (13-25 [/.), 
and has a wider ectoplasm. 

Genus Nagleria, Alexeieff (emend Calkins). 

Synonyms : 

Amoeba Umax Alexeieff. 
Vahlkampfia species Chatton. 

This genus, including a number of limax forms, was established by 
Alexeieff to include all of the questionable minute amoeboid forms 
which Chatton earlier included in his genus Vahlkampfia. Amongst 
these, however, were some species in which the life history on agar 
involved a change from the amoeboid to the flagellated stage, and 
vice versa. This is a distinct characteristic of generic value, and 
until similar flagellated stages are demonstrated in all species of 
Vahlkampfia they should be kept separate in classification. I have 
adopted Alexeieff's generic name 3 therefore, to include these limax 
forms, with a facultative flagellated stage. 

Whitmore (1911) still earlier described an amoeba from Manila 
with a flagellated stage in which three flagella were present. He 
named it Trimastigamoeba philippinensis. It is unfortunate that 
such a generic name should have been' given to this type, for in the 
first place it is not a mastigamoeba (which is the generic name of a 
flagellate), and in the second place the prefix makes it inapplicable to 
the biflagellated types. Hence we must include it as a subgenus 
provisionally or else place the biflagellated forms under the inappro- 
priate name of Trimastigamoeba. It may be better in the long run 
to place all amoeboid forms with flagellated stages under one generic 
name, in which case both Trimastigamoeba and Nagleria would be 
supplanted by Schaudinn's name Paramoeba. Until the life history 
of more species is fully known I think the latter course inadvisable, 
and will treat the uniflagellate, biflagellate, and triflagellate forms 
as different genera. 

Generic characters.- —Small Umax-Like forms with no essential mor- 
phological differences from Vahlkampfia, except for the fact that the 
adult amoebae acquire and lose flagella under conditions not fully 
recognized. They are viable, possess one contractile vacuole and a 
single nucleus of the limax type. The flagellated stage with definite 
oval form. Nuclear division promitotic; division of the flagellate 
stage unknown in the majority of cases. • 


Niigleria punctata Dangeard. 

Dangeard, P., 1910. Etudes Sat le developpement et la structure des organ- 

isnies inferieurs. Le Botaniste Vol. 2. 
Wasielewsky und Hirschfeld, 1910. Untersuchungen uber Kulturamoben. 

Abh. Heidelberg. Ak. Bd. 1. 

With the characters of the genus. Size about 25ja; nucleus with 
a distinct karyosome; flagella two in number, equal in length and 
about as long as the cell body. The nucleus of the flagellated forms is 
at the anterior end of the cell near the base of the flagella, while the 
contractile vacuole is posterior. Cysts uninucleate, smaller than the 
adults. Division promitotic. Habitat pond water. 

Wasielewsky and Hirschfeld, 1910, have described somewhat simi- 
lar flagellated stages in an amoeba from hay and in one from tan 

Genus Paramoeba Scbaudinn. 

Schaudinn, F,, 1S96, Ueber die Zeugungkreis von Paramoeba Eilhardi. 

This genus was created by Schaudinn for an amoeba found by him 
in a salt-water aquarium. It is characterized by a peculiar relation 
of nucleus and accessory body which Schaudinn called the Neben- 
korper. The latter divides first into many parts and then the nucleus 
divides into as many parts as there are portions of the Nebenkorper. 
The genus is further characterized by the formation of swarmers 
with two flagella, two chroma tophores and a pigmented " eye-spot " 
or stigma. The flagellates increased by longitudinal division recall- 
ing in morphology and division the small flagellate Cryptomonas. 
The observations need confirmation. Paramoeba eilhardi Schaudinn. 
The single species known, with the characters of the genus. 

Genus Craigia Nov. gen. 

Craig, 1906, observed a small amoeba in the human intestine in six 
cases of chronic diarrhoea. He named it Paramoeba hominis because 
of the presence of an accessory body which he compared with the 
Nebenkorper of P. eilhardi and the formation of flagellated swarmers. 
The identity of the accessory body with the Nebenkorper is question- 
able while the single flagellum of the swarmers is sufficient to throw 
it out of the genus named by Schaudinn. For these reasons I propose 
to give it a new generic name — Craigia — after its discoverer. 

Generic characters. — Small, free-living or parasitic amoebae with 
a uniflagellated swarmer stage. Amoeba stage from 10-25jjl with 
little differentiation into ectoplasm and endoplasm when quiet but 
with anterior ectoplasm in movement. The endoplasm with or with- 
out an extrannclear body recalling the Nebenkorper of Paramoeba. 
The flagellated stage with a single flagellum. 


C. hominis Craig. 

Synonym : Paramoeba hominis Craig. 

Cm is, C. F., 1900. In Amor. Jour, of the Med. Sciences, 1906. 
Cniig, C. F., 1910. Further Observations on Paramoeba hominis, an [ntestlnal 
Parasite of Man. Arch, of Intern. Med. Vol. 6, p. 1. 

With the characters of the genus. Endoplasm granular with acces- 
sory body interpreted by Craig as Nebenkorper, but this is not satis- 
factorily demonstrated. Flagellated form smaller than the amoebic 
stage (10-20[jl), spherical with slight conical protuberance at the 
base of the flagellum. Multiplication of the flagellates by longi- 
tudinal division, including division of the motile organ. Cysts from 
15— 18jj. in diameter, spherical, with the usual double membrane. 
Reproduction by simple division in amoebic and flagellated stages, 
and by swarmer-formation within the cysts. Habitat human intes- 
tine, where it possibly causes a chronic diarrhoea. Confirmation 

('. pigmenlifera Grassi, 1881. 
Synonym : 

Paramoeba pigmentifera Janicki. 

Amoeba pigmentifera Grassi. 
Grassi, G. B. See following bibliography. 
Janicki, C. See following bibliography. 

Small forms only 30ja in diameter. Movement slow, endoplasm 
highly granular, ectoplasm visible only at point of pseudopodia 
formation. The nucleus is difficult to see in life. Nebenkorper larger 
than the nucleus and covered with a black pigment. Flagellate stage 
with a single flagellum, Nebenkorper and nucleus. As in Paramoeba 
eilhardi the flagellates reproduce by division (Janicki). Body cavity 
of Chaetognatha. 

G. chaetognathi Grassi. 

Synonyms: Amoeba chaetognathi Grassi. Paramoeba chaetognathi Janicki. 

Grassi, G. B., 1881. Intorno ad alcuni protisti endoparassitici, etc. Atti Soc. 
Ital. Sc. Nat. Vol. 24. 

Janicki, C, 1912. TJntersuchungen an parasitischen Arten der Gattung Para- 
moeba Schaudinn. Verh. d. Naturf. Ges. in Basel. Bd. 23. 

Smaller form than the preceding (18jjl). Protoplasm and inclu- 
sions similar to those of the preceding. Nebenkorper not visible in 
life. Flagellate stage similar to the preceding. Life history un- 
known. Body cavity of Chaetognatha. 

Genus Trimastigamoeba Whitmore. 

Single species T. philippinensis Whitmore. 

Whitmore, E. R.. 1911. Studien iiber Kultur.unoben. Arch. f. Prot. Vol. 23. p. 81. 

Amoeboid form of Umax type from 16—18^ in diameter. Ectoplasm 
not distinct from endoplasm, except in advancing pseudopodium. 
Contractile vacuole present in posterior end of body. Ordinary vege- 


tative forms change into flagellated forms. The latter have three 
equal flagella. are oval and elongate from 16—22^ in length with 
nucleus in the anterior end. Habitat tap water, Manila. 

Genus Entamoeba, Leidy. 
Synonyms : 

Amoeba Lqesch. 

Endamocba Leidy. 

Entamoeba Casagrandi and Barbagallo. 

Loschia Chatton. 

Proctamoeba (Alexieff) (in part). 

The present genus was established by Leidy in 1879, although with 
slightly different orthography, the name given by him being Enda- 
moeba. The significance is identical, and Leidy therefore should 
have credit for the name. In this country we use the form end 
rather than ent for terms like endoderm, endoplasm, etc., while in 
Europe the form is entoderm, entoplasm, etc. Without considering 
the academic question as to which form is the more accurate, the fact 
remains that endamoeba was the original name, Casagrandi and Bar- 
bagallo in 1897 using the form entamoeba without reference to 
Leidy's priority. We agree with Chatton therefore in crediting 
Leidy with the generic name, but accept the form given by Casa- 
grandi and Barbagallo and adopted by Schaudinn. 

A great deal of a priori reasoning has been invoked to prove that 
all pathogenic and parasitic forms of amoeba are not viable on 
protozoan agar or other culture media, while, on the other hand, 
cultivated forms from diseased entera are often dismissed as being 
free-living forms which in the encysted state have passed through 
the alimentary tract without entering upon the vegetative stages. 
On purely a priori grounds, however, and with the possible exception 
of E. histolytica and tetragena, there is no reason why parasitic 
forms should not be cultivated on agar. Nor, on the other hand, is 
there any reason why free-living forms should not become adapted 
to life on bacteria in the digestive tract, since this is the only obvious 
way in which pathogenic forms originally must have acquired their 
parasitic mode of life. We must seek some other means than 
viability for identifying parasitic and pathogenic forms from those 
which are normally free living, and here, as in all other kinds of 
protozoa, the full life history must first be known. In lieu of this, 
the differences in morphology, especially of nuclei, mitotic figures, 
and crysts may be provisionally accepted. 

Generic characters. 

Commensal, parasitic, or pathogenic amoeba living a vegetative 
life in the digestive tracts of different animals from man to lower 
invertebrates. Size usually small (from 10 to 50[x) ; ectoplasm more 
or less well defined; endoplasm clear, or finely granular, or with 
large granules of volutin, or with chromidia. Contractile vacuoles 


usually absent. Nuclei vesicular with or without definite karyosomes. 
Nuclear division mesomitotic or mitotic. Reproduction by simple 
division, by budding, or by spore formation. Life history known 
in only a few forms; sexual processes autogamic when known. Com- 
mensal forms probably viable; cytolytic forms probably not. 

Type species Entamoeba blattae Biitschli, 1878. 

IJiUsclili, O. 1878. Beitriige zur Kenntnis der Flagellaten u. einiger verwand- 

ten Organisinen. Zeit. wiss. Zool. Bd. 30, p. 205. 
Elmassian. 1909. Sur l'Amoeba blattae. Morphologie, Generation. Arch. f. 

Prot. Bd. 16, p. 143. 
Janicki, C. 1908, Contrib. alia canoscenza di alcuni Protozoi parassiti della 

Periplaneta orientalis. Atti d. Iteale Acad, dei Lincei. Vol. 17. 
Janicki, C. 1909. Ueber Kern und Kerntbeilung bei Entamoeba blattae Btit. 

Biol. Cent. Vol. 39, p. 381. 
Leidy, J. 1879. On Amoeba blattae. Proc. Ac. Nat. Sc. Philadelphia, Oct., 1879. 
Mercier, L. 1909. Le cycle evolutif d'Amoeba blattae But. Arch. f. Prot. Bd. 

16, p. 165. 
Mercier, L. 1910. Beitriige zur Kenntnis der Amoeba blattae u. A. proteus. 

Arch. f. Prot. Bd. 6, p. 1. 

Single individuals from 12-50u,, but may become much larger 
{*80-100[a). The living forms show little evidence of ectoplasmic 
differentiation, but the endoplasm is marked by fairly definite stria- 
ta ons. The single nucleus has a definite peripheral layer of chro- 
matin and a small karyosome. Multinucleate forms are also common. 
Contractile vacuoles numerous. Transparent multinucleated cysts 
are formed with from 20-30 nuclei. According to Mercier, these are 
gamete-forming cysts which give rise to minute uninucleate gametes 
which conjugate outside the cyst, the copula developing into the 
ordinary vegetative forms. Vegetative reproduction by simple divi- 
sion. Habitat, end gut of various species of cockroaches. 

E. ranarum Grassi, 1881. 

Synonym : Amoeba ranarum Grassi. 

Dobell, C. C. 1909. Researches on the intestinal parasites of frogs and toads. 

Q. J. M. S. Vol. 53, n. s. 
Grassi, G. B. 1881. See bibliography p. — . 

Size variable from very minute forms (buds ?) 3-5[j. up to a 
medium size of 20-40jji. and occasionally 60pi. Movement similar to 
that of limax forms. Protoplasm very fluid with many vacuoles 
and w T ith one spherical nucleus. Reproduction by simple division or 
by spore formation within a cyst, four spores being formed (Dobell). 
Hartmann describes an autogamous sexual cycle. Habitat stomach to 
end gut of frogs. 

E. testudinis Hartmann. 

Hartmann, M. 1910. Ueber eine neue Darmamoebe. E. testudinis. Mem. do 
Institute Oswaldo Cruz. Vol. 2. 

Size from 5O-70pi. Ectoplasmic differentiation distinct. Endoplasm 
filled with vacuoles and food particles in various stages of diges- 


tion. Nucleus visible in life, from spherical to oval shape, with 
fine peripheral granules of chromatin, central spongy mass corre- 
sponding to a karyosome, and a distinct nuclear membrane. Repro- 
duction unknown. Habitat, digestive tract of turtle. 

E. buccalis Prowazek. 
Synonyms : 

Amoeba buccalis Steinberg. 

Amoeba pulmonalis Artault. 
Prowazek, P. 1904. Entamoeba buccalis. Arbeit, a. d. Kais. Gehundheits. Bd. 21. 
Leyden, 1905. In Lowentbal Entamoeba buccalis Prow, in einem Fall von 
Carcinom des Mundbodens. Cbarite Annalen Bd. 29. 

Small active forms from 6-32[a. Ectoplasm and endoplasm differ- 
entiated when organisms are at rest. Endoplasm filled with gastric 
vacuoles; contractile vacuole absent. Nucleus small, with karyo- 
some, centriole and peripheral chromatin. Nuclear division evi- 
dently promitotic, but not sufficiently studied for definite statement. 
Spore formation probable. Habitat carious teeth; also found in 
mouth carcinoma, and possibly in lungs (Artault 1898, A. pulmon- 

E. Kartulisi Doflein. 

Synonym : E. mawillaris Kartulis. 

Doflein, F. 1901. Die Protozoen als Parasiten und Krankbeitserreger. 

Doflein, F. 1911. Lebrbucb der Protozoenkunde. 

Size from 30-38[a. Ectoplasm not clearly differentiated; endo- 
plasm filled with large granules. Movement active with long finger 
formed pseudopodia recalling the " tentacles of a snail." Nucleus 
small with definite karyosome, not visible in life. Contractile vacuole 
absent. Reproduction unknown. Habitat, man; first found in a 
tumor of the lower jaw in Egypt (Kartulis) and in America (Flex- 
ner). The organisms occur not only in the abscess fluid but also in 
the deeper bony tissues. Possibly related to E. histolytica. 

E. urogenitalis Baelz. 

Balz, 1883. In Berliner klin. Wocbenscbr., p. 237. 
Jurgens, 1892. In Deutsch. mediz. Wocbenscbr., p. 454. 

Kartulis, 1893. Ueber patbogene Protozoen bei dem Menscben. Zeits. Hyg. 
und Inf. Bd. 13, p. 2. 

Posner, 1893. Ueber Amoben im Harn. Berlin Klin. Wocbenscbr. Bd. 30, p. 674. 
Size from 22-50pi. Movement slow by means of short pseudopodia. 
Endoplasm highly granular with one or more nuclei. Red-blood 
corpuscles also found in endoplasm. Reproduction unknown. Habi- 
tat mucous membrane of the human bladder. Possibly related to 
E. histolytica. 


E. histolytica Schaudinn. 

Synonym: Amoeba dysenteriae Councilman ;iI| d Lafleur. 

Schaudinn, F. 1903. See bibliography p. — . 

Craig, C. F. 1912. See below p. — . 

Since Councilman and Lafleur's description of "Arruxba dysen- 
teriae " was inadequate to enable us to distinguish to-day the organ- 
ism with which they worked, we accept the subsequent names " his- 
tolytica " and "tetragena " given by Schaudinn and Viereck. This 
was the first amoeba to be distinguished as pathogenic from the 
harmless E. coli by the careful observations and experiments of 
Schaudinn. Like E. tetragena,, it is a cause of pernicious or tropical 

Many recent observers claim that histolytica and tetragena are 
the same ; others, notably Craig, find a distinct difference in appear- 
ance and life history. 

Size from 20-30[j. (Doflein), 10-70> (Craig). Movement active 
by means of blunt or finger formed pseudopodia which are refrac- 
tive and clearly distinguished from the rest of the cell. Endoplasm 
granular and contains numerous vacuoles and ingested red-blood 
corpuscles when the latter are present in the fa3ces. Contractile 
vacuole absent. Nucleus difficult to see in life, contains but little 
chromatin, and has a minute karyosome. It is ex-centric in position, 
usually lying against the cell membrane. A definite nuclear mem- 
brane is absent. Reproduction by simple division, by budding, and 
by permanent spore formation. The latter are formed by budding, 
contain chromidia and are covered by a brown cyst wall. Life his- 
tory still unknown. Habitat, human digestive tract, causing acute 
enteritis and abscess formation in various organs. 

E. tetragena Viereck. 

Synonyms : 

Entamoeba africana Hartmann. 
Viereckia tetragena Chatton. 

Chatton, E. et Lalung-Bonnaire 1912. Amibe limax (Vahlknmpfia n. gen.) 
dans l'intestin humain. Bull, de la Soc. de Path. Exot. Vol. 5, p. 135. 

Craig, C. F. 1911. Entamoeba tetragena as a cause of Dysentery in the Philip- 
pine Islands. Arch, of Intern. Med. Vol. 7, p. 362. 

Hartmann and Prowazek. 1907. Blepharoplast. Karyosom nnd Centrosom. 
Arch. f. Prot. Bd. 10. p. 312. 

Viereck, H. 1906. Ueber Amobendysenterie. Med. Klinik. 1906. No. 41. 

Viereck, H. 1907. Studien (iber die den Tropen erworbene Dysenteric Arch, 
f. Schiffs. und Tropenhyg. Bd. 2. Beiheft 1. 

According to recent research this seems to be the most common 
cause of tropical dysentery. It measures from 8— 60pL, has lobose or 
finger-formed pseudopodia, which are distinctly refractile and well 
differentiated from the rest, of the cell. Endoplasm granular and 
contains red-blood corpuscles when the latter are present in the 
faeces. The nucleus is distinctly visible in life and has a definite 


double-contoured membrane lined by chromatin. A large karyosome 
is present and a distinct centriole. Reproduction by simple division 
and by spore formation preceded by autogamous fertilization. The 
result of fertilization is the formation of cysts with four amoeboid 
uninucleated spores. The latter number is the chief distinguishing 
feature between tetragena and E. coli, the latter having eight spores. 
The vegetative characters are so similar to those of E. histolytica 
that, until the life history of the latter is known, some doubt must 
still remain as to its specific difference. If this history shows iden- 
tity between the two, then the name tetragena must be abandoned 
and histolytica retained. Habitat, human intestine, causing acute 
tropical dysentery. 

E. coli, Losch, emend Schaudinn. 

Synonyms : 

Amoeba coli Losch. 
Amoeba lobospinosa Craig. 

Casagrandi and Barbagallo, 1897. Entamoeba hominis, etc. Ann. Ig. sperim. 
Vol. 5, p. 103. 

Craig, C. F. 1912. Observations upon the Morphology of Parasitic and Cul- 
tural Amoebae. Jour. Med. Res. Vol. 26, No. 1. 

Kartulis. 1905. Die Amobendysenterie. Kolle u. Wassermann Handb. d. 
Pathog. Mikroorg. 1 Erg. Bd. p. 347. 

Bosch, F. 1875. Massenhafte Entwickdung von Amoben im Dickdarm. Virch. 
Arch. f. pathog. Anat. Bd. 65. p. 196. 

Schaudinn, F. 1903. Untersuchungen uber die Fortpflanzung einiger Rhizo- 
poden. Arb. a. d. Kais. Gesundheitsamte Bd. 19. 

Average size from 25-35[a, but varies from 7-70pi. Movement is 
sluggish by protrusion of small blunt pseudopodia not well differen- 
tiated from the rest of the cell. General appearance glassy or trans- 
parent and with a gray tone. The endoplasm is finely granular with 
noncontractile vacuoles. Reproduction by simple division, or by 
multiple division, in which the nucleus fragments into eight parts, 
each part becoming the nucleus of an amoeboid spore. Fertili- 
zation autogamous, resulting in cyst formation, each cyst containing 
eight nuclei. After infection of a new host these amoeboid germs 
emerge from the cyst as minute amoeboid swarm spores. The cysts 
measure about 15\l. Habitat, human intestine, where, as a harmless 
commensal, it lives on bacteria. 

E. muris Grassi. 

Synonym : Amoeba muris Grassi. 

Grassi, G. B. 1881. See bibliography p. — . 

Wenyon, C. W. 1907. Observations on the Protozoa in the Intestine of Mice. 
Arch. Prot. Suppl. 1, p. 109. % 

Small forms up to 40>. Movement slow or rapid, according to 

temperature. Pseudopodium formation of the Umax type. Ecto- 

plasmic layer narrow and distinctly visible only in the pseudopodium. 

Endoplasm granular with large gastric vacuoles containing a variety 


of food matters. Nucleus visible in life; it is spherical and has a 
thick membrane. The chromatin is scanty and distributed as 
granules about the periphery. A karyosome lies in an achromatic 
network. Reproduction by division and by sporulation within cysts. 
The latter are spherical or oval, from 12— 14jjl in diameter. Matura- 
tion and autogamous fertilization occur within the cyst, resulting in 
eight nuclei, which probably form the nuclei of eight spores. 
Habitat, intestine and coecum of the mouse. 

E. Intestinalis Walker, 1908. 
Walker, E. L. 1908. See below. 

Williams, A. W. 1911. Pure Cultures of Amoebae parasitic in Mammals, 
Jour. Med. Res. Vol. 25\ p. 263. 

Medium-sized forms of the coli type. Ectoplasm and endoplasm 
distinct ; nucleus with large karyosome which furnishes the chromatin 
of the nuclear plate. Division of the nucleus mesomitotic. Highly 
phagocytic, red-blood corpuscles taken up with avidity. Reproduc- 
tion by division and by budding. Life history unknown. Habitat, 
intestine of rabbit and dog. Viable. 

E. cobayae Walker, 1908. 

Walker, E. L. 1908. The parasitic Amoebae of the Intestinal Tract of Man 
and other Animals. Jour. Med. Res. Vol. 17, p. 445. 

Similar in all respects to E. intestinalis. Habitat, intestine of 
guinea pig. Viable. 

Note. — In the review of species given above it is probable that a 
number of types have been omitted or overlooked. If such is the case 
I apologize in advance and plead that no slight has been intentional, 
the absence of literature, especially in medical journals, making itf 
impossible to cover the entire field in the short time at my disposal. 
A mere glance through the preceding pages shows the need of a 
modern and thorough monograph of the free and parasitic amoebae, 
and the writer will be very glad to undertake such a monograph if he 
can have the cooperation of the various students of the group. 


By Dr. Gary N. Calkins, 
Professor of protozoology, Columbia University, New York City. 

The time is now past when one or a few individuals of protozoa 
suffice to justify the publication of a new species or a description of 
normal processes. To-day the protozoologist, no less than the cytolo- 
gist working in cellular biology, must base his conclusions on vital 
activities or structural peculiarities of protozoa upon the study of 
66692— vol 2, pt 1—13 20 


thousands of cells. To obtain these, " cultures " are necessary, and 
the development of cultural technique is one of the most recent lines 
of work in protozoology. 

There is the greatest latitude in the use of the word culture as 
applied to protozoa. In general, it signifies an accumulation of one 
species under environmental conditions favorable for the active 
growth and multiplication of that species, but we frequently hear the 
term used to mean a rich collection of protozoa of many kinds. Very 
often Ave find, in natural waters or infusions, vast numbers of a 
single species ; such " natural cultures " are eagerly sought by the 
protozoologist and quantities of " material " of Noctiluca or Peridin- 
ium in sea water, or of Colpidium, Paramecium, Vorticella, Spirosto- 
mum, Chilomonas, and other forms of ciliates and flagellates are thus 
obtained. Such " natural cultures," however, make of the protozoolo- 
gist too much of an opportunist and " artificial culture " methods 
have been devised to supply the demand for quantities of material 
at will. 

The secret of making artificial cultures consists in finding the 
appropriate food of the organism to be studied. When such food is 
the bacteria of pond water, for example, the problem is simple, and 
tens of thousands of Colpidium, Paramecium, Vorticella, Stylonychia, 
etc., can be raised from one individual in a few weeks. When the 
food is specific, the difficulty is greater. Then food habits must be 
studied and the specific food required raised in abundance. In this 
way we have learned to cultivate ciliated protozoa of many kinds — 
Didinium on Paramecium, Spathidium on Colpidium, Actinobolus 
on Halteria, etc. — through hundreds of generations. 

It may be stated without exaggeration that probably every type 
of protozoa can be cultivated artificially, and this generalization 
applies in the case of our present subject, Amoeba. Experience 
has shown that with these rhizopods, as with the infusoria, some lend 
themselves readily to the culture methods, while others, thus far, 
have given negative results. This is true of the largest and finest 
specimens of amoebae, viz, A. proteus, A. vespertilio, A. ftava, etc. 
Nevertheless, these forms frequently appear in great abundance in 
" natural cultures," and it is only a matter of time and research to 
discover the conditions under which they thrive. 

Amoebae which have been cultivated on artificial media have been 
in all cases those forms which normally feed on bacteria. The methods 
of cultivation, especially in the hands of the bacteriologists, have 
become more and mora perfected until now it is possible to obtain 
"pure cultures" of certain types. Williams (1911) distinguishes 
three types of amoeba cultures as 1, mixed cultures; 2, pure mixed 
cultures; and 3, pure cultures; and full accounts of the many methods 
that have been employed in getting such cultures may be found in 


the works of Behla (1898), of Vahlkampf (1906), Musgrave and 
Clegg (1906), and Walker (1908). 

Mixed cultures of amoebae have furnished material for study since 
the time of Auerbach, in 1856, but until comparatively recent years 
little effort was made to study a single species. This became pos- 
sible when "pure mixed cultures" were used in which a single strain 
of amoeba was grown with a single species of bacteria as food. The 
great majority of papers on the cultivation of amoebae have been 
based upon this type of culture, which from the zoological standpoint 
is perfectly satisfactory. A common way of starting cultures of 
water-dwelling amoebae is to seed sterile straw or hay infusions with 
specimens of the amoeba desired. This was the method of Auerbach 
and the earlier investigators. A better way is to seed the desired 
amoebae on some gelatinous medium, such as agar or gelatine, to 
which sterile hay or straw infusion may be added. The amoebae grow 
in the water of condensation or on the more solid substance, from 
which they can be picked out and transplanted until " pure mixed 
cultures " result. In general a medium should be employed on which 
bacteria do not grow rapidly. Casagrandi and Barbagallo, in 1898, 
found that Fucus crispus, 5 per cent strong, when made distinctly 
alkaline, keeps bacteria down and gives a good medium for many 
kinds of amoebae. They found that Entamoeba coli and E. blattae, 
however, would not grow on such media, and came to the conclusion 
that " only free-living amoebae having a contractile vacuole " can be 
grown in artificial cultures. Frosch, in 1898, cultivated earth amoebae 
(limax type) on a variety of media, the most satisfactory consisting 
of \ gram agar, 10 grams alkaline bouillon, and 90 grams water. 
Tsujitani (1898) made successful cultures on a medium consisting of 
1 to 1.5 grams agar, 20 grams nutrient bouillon, and 80 grams water. 
This was filtered, made alkaline, and sterilized. 

The results of these earlier workers showed in general that a num- 
ber of artificial nutrient media may be suitable for the cultivation of 
amoebae; that a certain alkaline reaction is necessary; and, appar- 
ently, that bacteria are absolutely necessary. The latter conclusion, 
however, was weakened by the observation of Tsujitani, who found, 
in 1898, that one species of amoeba would grow on the dead bodies of 
one species of bacteria. 

Vahlkampf, somewhat later, pointed out that the number and 
variety of media on which amoebae would grow are practically un- 
limited, and that too much stress is often laid upon the exact com- 
position, and even upon the alkalinity, an acid reaction, in some cases 
giving satisfactory results. He used a number of media, both fluid 
and solid, getting favorable results with all in connection with his 
excellent studies on Vahlkampfia (Amoeba) Umax, the first of the 


free living limax types to be carefully and accurately studied. He 
used as solid media the following combinations : 

1. Heyden Nahrstoff, 1 to 2 grams ; agar, 1.5 grams ; tap water, 100 grams. 

2. Somatose, 1 to 2 grams; agar, 1.5 grams; tap water, 100 grams. 

3. Nutrose, 1 to 2 grams; agar, 1.5 grams; tap water, 100 grams. 

4. Witte's peptone, 1 to 2 grams; agar, 1.5 grams; tap water, 100 grams. 

5. Agar, 1.5 grams; tap water, 100 grams. 

6. Fucus crispus, 5 grams; tap water, 100 grams. 

The bacteria used by Yahlkampf were Bac. subtilis, alvei, 
tumescens, and B. asterosperus. The best results were obtained by 
seeding in shallow Petri dishes which permit of daily microscopical 

The standard present-day agar-method of making pure mixed 

cultures was successfully used by Musgrave and Clegg (1904), and 

is now generally employed. The medium is made up as follows : 

Agar, 20 grams; Witte's peptone, 1 gram; Liebig's beef extract, 0.1 gram; 
sodium chloride, 1 gram; distilled water, 1,000 grams. 

These are dissolved by boiling or by autoclaving, and then made 
1 to 1.5 per cent alkaline by titration to phenolthalein, using sodium 
hydrate. This is cleared with the whites of two eggs and filtered. 
The filtrate is sterilized and tubed, and is ready for use either as 
slants or in Petri dishes. The surface is streaked with the material 
containing the desired amoeba and left in room temperature. 

In place of agar, some observers find albumen water an excellent 
medium. Behla, in 1898, described some early work by Balsamo 
Crivelli and Maggi, who cultivated an amoeba (which they called 
A. albuminis) on a nutrient medium of albumen, with or without the 
addition of weak carbolic acid. He further quotes Rina Monti, who 
used a similar medium consisting of a solution of albumen in dis- 
tilled water, two parts albumen to one of water acidified by carbolic 
acid. Quite recently Gliiser has had excellent results with free living 
amoebae by using a few drops of albumen (2 to 3) in a 6 cm watch 
crystal of tap water into which a piece of agar with amoebae is 
dropped. Enormous quantities of amoebae were obtained in three 
days at room temperature. Glaser does not recommend this for pure 
culture work, but, for cover glass smears with thousands of amoebae, 
he regards it as superior to solid media cultures. 

A number of limax types, capable of living on agar, pass into a 
flagellated stage. Such forms have been described by Wasielewsky 
and Hirschfeld in 1910, by Whitmore in 1911, and by Alexeieff in 
1912. The former used an albumen medium and Whitmore the alka- 
line agar method of Musgrave and Clegg; the latter finding that 
flagellated stages of his Trimastig amoeba philippinensis could be 
raised from the ordinary cysts and vegetative forms by flooding his 


agar plates with a few cubic centimeters of tap water, the swimming 
forms appearing in about 2 hours, becoming very numerous in 4 
hours, and returning to the amoeboid phase after 20 hours. 

Although " pure mixed cultures " are perfectly satisfactory for the 
ordinary amoeba culture, the question arises: Can pure cultures in a 
bacteriological sense be made and continued in transplant genera- 
tions ? A number of a priori arguments have been raised against the 
possibility of this result. Vahlkampf expresses these objections very 
clearly, pointing out that amoebae — typical animals — can not live 
on dissolved proteids and salts in the surrounding medium, but must 
take their food in the complex form of proteids. He concludes that 
it would be impossible to get pure cultures or to raise them without 
their natural food-bacteria. On similar a priori grounds an answer 
to this would be that living proteid food is not necessary to supply 
the needs of animals, and, if dead organisms or parts of organisms 
could be engulfed and digested, pure cultures, in the sense of only 
one strain of living things, would result. Tsujitani, for example, 
has already been referred to as having cultivated one strain of amoeba 
on one species of bacteria used when dead. He does not mention 
transplants nor continued culture generations. This Avork was re 
peated and confirmed by J. T. Chase and A. W. Williams (see 
Williams, 1911), who succeeded in growing one strain of amoeba 
through 10 culture generations on agar cultures of dysentery bacilli 
killed by heating. Still more interesting is Williams's work with 
sterile extracted animal tissues rendered bacteria-free by special 
precautionary methods. Tissues of brain, liver, kidney, and other 
organs were placed on agar in a thermostat at 36° C for 24 hours; 
small quantities of the broken-up tissues were then mixed with the 
amoebae on agar plates. Usually in abundant growth or pure culture 
resulted in 24 hours at 36° C, or in from three to five days, at room 
temperature. In this way, Williams has cultivated Entamoeba coll 
(Musgrave and Clegg's strain 11524), Entamoeba intestinalis, E. 
cobayae, the first through 54 culture generations, the second through 
30 generations, and the third through 15 generations, at 36° C. up to 
the time her paper was written. The question of pure cultures, there- 
fore, in the light of her carefully guarded experiments seems to be 
well beyond the reach of adverse a priori criticism. 

The probability of cultivating pernicious forms of Entamoeba on 
artificial media is well established by Williams's results, and it bids 
fair to be only a matter of time before E. histolytica and E. tetragena 
will be raised in sufficient quantities for detailed study of all phases 
of their life history. 



Alexeieif, A. 1912. Sur less caracteres cytologiques et la systematique des 

amibes du groupe Limax, etc. Bull, de la Soc. Zool. de France. Tome 

Auerbach, L. 1856. Ueber die Einzelligkeit der Amoben. Zeit w. Zool., 1856. 
Behla, R. 1898. Amoben, insbesonders voin parasitaren u. kulaurellen 

Standpimkte, Berlin. 
Casagrandi and Barbagallo. 1898. Ueber die Kultur von Amoben. Cent. f. 

Bakt., Bd. XXI. 
Frosch, P. 1898. Zur Frage der Reinzuchtung der Amoben. Cent. f. Bakt., 

Bd. XXI. 
Gliiser, H. 1912. Untersuchungen iiber die Teilung einiger Amoben. Arch. 

f. Prot, Bd. XXV. 
Musgrave and Clegg. 1904. Amebae, their cultivation and etiologic signifi- 
cance. U. S. Bur. of Gov. Lab. Biol. Lab. No. 18. 
Tsujitani, J. 1898. Ueber die Reinkultur der Amoben. Cent. f. Bakt, Bd. 

Vahlkampf, E. 1905. Beitriige zur Biologie und Entwicklungsgeschichte 

von Amoeba Umax, etc. Arch. f. Prot., Bd. V. 
Walker, E. L. 1908. The parasitic Amebae of the Intestinal Tract, etc. Jour. 

Med. Res., Vol. XVII. 
Wasielewsky and Hirschfelt. 1910. 
Whitmore, E. R. 1911. Studien iiber Kulturamoben aus Manila. Arch. f. 

Prot, Bd. XXIII. 
Williams, A. W. 1911. Pure Cultures of Amoebae parasite in Mammals. Jour. 

Med. Res., Vol. XX. 



By Dr. Victor C. Vatjghan, University of Michigan, Ann Arbor, Mich. 


Studies of the phenomena of protein sensitization, so-called ana- 
phylaxis, have given us quite a new idea of many of the problems 
of immunity and disease. The only way in which cells of any kind — 
bacterial, protozoal, or animal — can grow and multiply is by elaborat- 
ing ferments which split up the pabulum within their reach, thus 
preparing a food supply. The cell which can no longer supply a 
digestive ferment is already dead, whatever be the kind or amount 
of pabulum surrounding it. The cell which supplies only such fer- 
ments as can not digest the food supply within its reach dies imme- 
diately. This is the fundamental fact of the general immunity pos- 
sessed by higher animals against the lower forms of life. As was 
shown in my laboratory some years ago, there is no constant and fixed 
relation between the toxicogenic and pathogenic properties of bacilli. 
The bacillus prodigiosus contains enough intracellular poison to kill 
guinea pigs when injected intraperitoneally in doses of 1 : 90,000 body 
weight, while the anthrax bacillus requires 1 : 1,700, and still the 
former is nonpathogenic and the latter highly pathogenic. The 
explanation lies in the fact that the prodigiosus can not grow and 
multiply in the animal body because its secretions do not digest the 
proteins of the animal body, or, what is more probable, the secretions 
of the body cells destroy the bacillus. On the other hand, the an- 
thrax bacillus elaborates ferments which do digest the proteins of 
the animal body, while the body cells do not destroy the bacillus, and 
thus serve the microorganism with food. For these same reasons a 
given bacillus may be pathogenic to one species or to one race and 
wholly devoid of effect on other animals. Furthermore, the viru- 
lence of different strains of the same microorganism varies with the 
abundance and the strength of the digestive ferment. One strain of 
the pneumococcus may not kill guinea pigs in less doses than 1 cubic 
centimeter of a 24-hour culture, while another may kill in one- 
millionth of this amount, and still when animals inoculated with the 



two strains are dead the same number of bacilli or the same amount of 
bacillary cell substance will be found in both. One strain has multi- 
plied a million times faster than the other because of the greater 
abundance and effectiveness of the secretions which enable it to 

The great lesson which we have learned from our studies of ana- 
phylaxis is that the digestive secretions of body cells may be devel- 
oped and modified by the kind of protein brought into contact with 
them. When a foreign protein is introduced into the animal body 
certain cells develop a specific digestive ferment which splits up that 
protein and no other. Cellular digestion is a physiologic process 
and it is normally specific inasmuch as the secretion of each kind of 
cell splits up the pabulum in such a way as to supply the needs of its 
own cell, but the pabulum upon which the cells of the body normally 
feed consists of the proteins of the blood and lymph. From these 
sources all the cells of the body select their food material through the 
agency of their digestive ferments. Normally there is much prep- 
aration of the foods upon which the cells of the animal body feed. 
The proteins taken into the alimentary canal are broken up by the 
digestive juices into amino acids, and in this process they lose all 
their distinctive character. During absorption or soon thereafter the 
amino acids are put together again, but now so grouped as to form 
the proteins peculiar to the species. From the special proteins thus 
prepared each kind of body cell obtains its nutriment. Parenteral 
digestion is a physiologic process in which the material acted upon, 
the cleavage agents, and the assimilating cells are constant. How- 
ever, even with all this preparation of food for the body cells it must 
happen at times that foreign proteins, as such, find their way into the 
blood and lymph. In order to digest this unusual pabulum the body 
cells elaborate a specific ferment, which digests this protein and no 
other. This is one of the fundamental and central facts of protein 

The second fundamental fact in protein sensitization is that every 
protein molecule contains a poisonous group. This is true of all 
bacterial, vegetable, and animal proteins, so far as they have been 
investigated. The poisonous group in the protein molecule is the 
same so far as its physiological action is concerned, whatever be the 
nature of the entire molecule of which it is a part. Chemically there 
must be differences in the poisonous groups of different protein mole- 
cules, but, as has been stated, in physiological action one can not be 
distinguished from another. It may be that more exact studies will 
show slight variations in physiological effect. I have designated the 
poisonous as the primary group in the protein molecule. I have also 
suggested that it be regarded as the " archon " or keystone of the 


protein molecule. It probably contains the benzol ring with nitro- 
genous side chains. Attached to this primary group are secondary 
groups which may be designated as the " characteristic " groups, be- 
cause it is in these that one protein differs from another. The sensi- 
tizing properties of proteins reside in the secondary groups, because 
it has been shown that these, when freed from the poisonous group, 
may sensitize animals to the unbroken molecule. It is for this reason 
that the special ferments elaborated in the cells of the animal under 
the influence of a foreign protein are specific. The poisonous group, 
when detached from its secondary or characteristic groups, does not 
sensitize either to itself or to the whole protein from which it came. 
In the original protein molecule the poisonous group is rendered 
inert physiologically by being combined with the secondary groups. 
In its free state it becomes a poison on account of the avidity with 
which it disrupts other protein molecules and combines with their 
secondary groups. The protein molecule may be compared to a basic 
or neutral salt, and it becomes more and more poisonous as its basic 
elements are removed, and when the free acid only is left its maxi- 
mum toxic action is reached. The protein poison is a powerful agent, 
In the purest form in which I have been able to obtain it, and this 
probably is far from chemical purity, it kills guinea pigs of from 200 
to 300 grams weight, when injected intracardiacally in doses of 0.5 
milligram. When used intra -abdominally this dose must be multi- 
plied by 16, and when given subcutaneously by about 32. These 
differences in effect, according to the method of administration, are of 
importance and are accounted for by the fact that the poison attacks 
and is neutralized by the body proteins with which it first comes in 

Whenever neutral proteins undergo cleavage as the result of the 
activity of proteolytic enzymes there are steps in the process when 
the activity of the poisonous group is made more manifest, and this 
proceeds as the basic elements are stripped off. In this way the 
poison is in part liberated in alimentary digestion. Biedl and Kraus 
have shown that the action of the anaphylactic poison and that of 
pepton are identical. This is necessarily true because the active 
group in both is the same. The protein poison is set free or activated 
by the alimentary proteolytic enzymes, and, if it were a readily dif- 
fusible substance, all proteins would be poisonous to man when taken 
by the mouth. But since it does not speedily pass through the ali- 
mentary walls and since further cleavage renders it inert we escape its 
poisonous action. In parenteral digestion of proteins there are no 
walls to prevent the diffusion of the poison, and consequently more or 
less injury always results. 

Anaphylactic shock is such a striking phenomenon that for a long 
time it obscured the essential facts of protein sensitization and led 


investigators far astray. When compared with immunity, the two 
seemed antipodal. In one the life of the animal is saved ; in the other 
it is jeopardized, and, in the majority of instances, lost. Indeed, it 
was a misconception which led Eichet to select the term "anaphy- 
laxis." I still hold to the following statements concerning protein 
sensitization first formulated by Wheeler and myself i 1 

(1) Sensitization consists in developing in the animal a specific 
proteolytic ferment which acts upon the protein that brings it into 
existence and on no other. 

(2) This specific proteolytic ferment stored up in the cells of 
the animal as a result of the first treatment with the protein remains 
as a zymogen until activated by a second injection of the same 

(3) Our conception of the development of a specific zymogen 
supposes a rearrangement of the atomic groups of the protein mole- 
cules of certain cells in the animal body or an alteration of the 
molecular structure. In other words, we regard the production of 
the specific zymogen not as the formation of a new body, but as 
resulting from an alteration in the atomic arrangement within the 
protein molecule and a consequent change in its chemism. 

(4) Some proteins in developing the specific zymogen produce 
profound and lasting changes in molecular structure, while the alter- 
ations induced by others are slighter and of temporary, duration, 
the molecular structure soon returning to its original condition. 

(5) Bacteria and protozoa are living, labile proteins, while egg 
white, casein, serum albumin, etc., are stable proteins. The proteins 
of the one group are in an active and those of the other in a resting 
state, but both are essentially proteins, made up of an acid or poison- 
ous chemical nucleus and a basic or nonpoisonous group. The for- 
mer in its effects upon animals is the same whether derived from the 
living or the dead protein, and the latter in the one instance induces 
specific immunity and in the other specific susceptibility; but the 
immunity and susceptibility each consists in developing in the animal 
body the capability of splitting up a specific protein. If the living 
protein be split up before it has time to multiply sufficiently to fur- 
nish a fatal quantity of the poison, the animal lives and we say that 
it has been immunized. If the stabile protein be introduced into 
the animal, it leads to the development of a specific proteolytic 
ferment, and if enough of it to supply a fatal dose be reinjected 
after this function has been developed the animal dies. The first 
or sensitizing dose of egg white injected into an animal is digested 
just as surely as is the second, but the process goes on so slowly that 
we Bee no effect; but in fact the first dose has affected the animal 
profoundly, so profoundly that the change wrought in certain cells 
of the animal body persist for months, possibly for years, and may 


be transmitted from the mother to her offspring. We do not say 
that the animal is sensitized unless some immediate and striking 
effect follows our treatment, but this is wrong. An immediate effect, 
especially a fatal issue, on reinjection depends upon the rapidity 
with which the protein is split up and its poisonous constituent set 
free. The sensitizing injection leads to the development of a specific 
enzyme, and the protein of this injection is so slowly digested that 
the poison set free at any one time is not sufficient to produce any 
recognizable effect. If time enough be allowed between the sensi- 
tizing and the reinjection for the accumulation of a large amount 
of the specific enzyme, then the protein is split up promptly and 
anaphylactic shock and death result. These views concerning pro- 
tein sensitization, first offered in 1907, have been on the whole con- 
firmed by later investigators, generally without credit to those who 
originally proposed them. 

The fact that an animal is sensitized before the time when a rein- 
jection is followed by anaphylactic shock has been conclusively 
demonstrated by inducing passive anaphylaxis with serum taken 
from animals in the so-called preanaphylactic state. Likewise it 
has been shown that serum taken from animals in the so-called anti- 
anaphylactic state passively sensitizes fresh animals. 


From a practical standpoint anaphylactic shock is the least im- 
portant of the phenomena of sensitization. It is always an arti- 
ficially induced condition, and the only importance it brings to the 
practitioner is that he should know how to prevent it in serum 
therapy. Although the procedure necessary to protect the patient 
against anaphylactic shock was first pointed out by Vaughan, jr., the 
best work along this line has been done by Besredka. The last-men- 
tioned investigator has shown that the intraperitoneal injection of 
from one-fiftieth to one one-hundredth cubic centimeter of the serum 
in sensitized guinea pigs renders them so positively refractory that 
five hours later intracerebral injections are wholly without effect. 
Besredka has made quite a thorough study of the means by which 
anaphylactic shock in serum therapy may be averted, and he states 
his conclusions as follows : 

(1) Preparatory heating of therapeutic sera to 56° tends to sup- 
press the phenomena of sensitization without wholly averting them. 
Besredka states that all therapeutic sera prepared at the Pasteur 
Institute are subjected to this temperature, and that instances of ana- 
phylactic shock are less frequent, and, when seen, less severe in 
France than in countries in which this preliminary heating is not 


(2) Alcoholic and ether narcosis give a complete, but transitory, 
immunity to anaphylactic shock. (This is not practical.) 

(3) Preventive injections of serum heated to 80° produce a certain 
and lasting immunity, but it develops slowly and is accompanied by 
slight reaction. (It will be understood that only that portion of the 
serum used to prevent anaphylactic shock is heated to this tempera- 
ture, which would render antitoxin inert.) 

(4) The best method of averting anaphylactic shock is either by 
rectal injection of the unheated serum, or, better still, by the subcu- 
taneous injection of a very small dose. 

The recommendation of Vaughan, jr., is that in all cases in which 
anaphylactic shock may be feared a preliminary injection of from 
0.1 to 0.2 cubic centimeters should be made, and after an interval of 
two hours, provided no untoward symptoms have appeared, the full 
dose may be given. The suggestion is made by Kosenau and Ander- 
son that all individuals who have shown any tendency to asthma, to- 
gether with those who have received previous injections of the serum, 
with an interval of 12 days or longer, should be included among those 
in whom anaphylactic shock may be feared. It is not held that even 
with these precautions all the symptoms of serum disease will in all 
cases be averted, but serious anaphylactic shock is not likely to occur. 


The studies of v. Pirquet and Shick 2 on diseased conditions in- 
duced by therapeutic sera have proved of great value in explaining 
the phenomena of protein sensitization. In a certain per cent of 
individuals who receive injections of horse serum for the first time 
certain well-defined symptoms develop, usually from 6 to 12 days 
after the injection. The symptoms consist of fever, more or less 
general edema and rash, generally urticarial, though sometimes 
erythematous. The rash is usually accompanied by intense itching, 
and it may cover not only the entire surface of the body but extend 
to the visible mucous membrane of the mouth and throat, about the 
anus, and into the rectum. The lymph glands may be enlarged, and 
pain in the joints is often severe. The per cent of persons thus 
affected by the first dose of horse serum increases with the quantity 
of serum employed. The explanation offered by v. Pirquet is that 
some of the unchanged serum remains in the body until sensitization 
is sufficiently developed to "bring the effects of the toxic body up to 
the level of clinical observation." This demonstrates that a rein- 
jection is not necessary in order to develop the state of protein sensi- 
tization. The evolution of the specific enzyme begins soon after the 
introduction of the foreign protein and gradually proceeds, and the 
liberation of the protein poison increases parri passu. It is not until 


the effects of the liberated poison approach the " level of clinical 
observation " that we recognize them, but this is not at the beginning 
of the process. Sensitization of the body cell probably begins as 
soon as the foreign protein comes in contact with it. The foreign 
protein so impresses the body cell that the latter undergoes such 
changes in its intramolecular structure that it elaborates a new and 
specific enzyme. The fact that soluble proteins sensitize so much 
more promptly and efficiently than suspensions renders it probable 
that cellular penetration is essential to the most thorough effect. 
The additional fact that relatively dilute solutions sensitize more 
promptly and more efficiently than more concentrated ones suggest 
that degree of molecular concentration has some influence upon the 
processes of sensitization. 

Von Pirquet and Shick observed two kinds of reaction in those 
who received reinjections after intervals of 12 days or longer. In 
some the reaction is of the same character as that described above, 
but it appears two or three days earlier. It is supposed that those 
in whom this form, designated as " accelerated reaction," occurs 
have partially passed beyond the condition of sensitization, but 
easily resume it on receiving the reinjection. There seems to be no 
danger to life in either the " delayed " or " accelerated reaction." 
The one accompanied by marked danger to life is the " immediate." 
In this the effects manifest themselves within a few hours, often 
within a few minutes after the reinjection. These individuals are 
in a fully sensitized condition, and it is in these that anaphylactic 
shock should be feared. 

There are instances in which the first injection of horse serum has 
induced alarming, and rarely fatal, anaphylactic shock. These have 
been reported with sufficient frequency to cause more or less anxiety 
in the employment of therapeutic sera; besides, it raises the very 
important question as to why a small per cent of persons should be, 
apparently naturally, susceptible to an agent to which the great ma- 
jority are immune. Cases of " horse asthma," in which more or less 
violent symptoms, such as sneezing, inflammation of the conjunctiva 
and the mucous membrane of the upper air passages, result from 
riding behind horses, are well known. The flying hairs from horses 
carrying minute quantities of protein are inhaled and may cause 
local sensitization, and it may be that this accounts for the instances 
of anaphylactic shock observed after first injections of horse serum. 


The valuable research of v. Pirquet 3 on vaccinia has done much 
to elucidate the problems of sensitization. We quote the following 
from one of his later communications on this subject : * 


" The first vaccination in healthy children shows an extremely constant symp- 
tom complex. Some minutes after the vaccination, a traumatic reaction, in 
the form of a very slight redness, appears, which lasts about one day, and leaves 
a small scab surrounded by normal skin. On the third or fourth day a small 
red papule appears, which indicates the beginning of the specific reaction. 
Between the fourth and sixth days, the middle portion of the papule becomes 
more elevated (papilla formation), the outer part becomes flat and forms a 
small red circle then the ' aula ' around the papilla. From now on the papilla 
increases in size quite regularly, about one millimeter a day, and the solid 
papule is transformed into a blister. The aula remains of the same size 
and is protruded only by the extension of the papilla. Between the eighth and 
eleventh days the aula increases to a large, slightly elevated plaque and ' area.' 
The papilla ceases to grow and becomes yellow. Between the eleventh and fif- 
teenth days the area reaches its highest development and then disappears slowly, 
whereas the papilla dries and a large scab falls off, leaving a scar." When 
daily vaccinations on the same person are made for a fortnight the papilla ap- 
pear in order corresponding to the day of vaccination, and the inflammation 
of the area appears on all the vaccination points simultaneously. "Although 
the vaccinations were made on successive days, the area develops around all 
the vaccination points at the same time ; that is, at the time when its develop- 
ment is due on the first vaccination points. From now on the papilla of the 
later vaccinations stop growing, as does the papilla of the first vaccination. 
In those vaccinations which have been made from this time on, the state of 
papilla formation is no longer reached. Another type of reaction occurs — 
" early reaction." In this reaction a papilla is formed, reaching its develop- 
ment in 24 hours and from then on gradually disappearing. 

The above nicely explains not only the development of vaccinia 
and the way in which it protects against smallpox, but also vaccina- 
tion in other infections diseases. The avirulent organism of vaccinia 
still has the protein constitution of the virulent one of smallpox. 
It has been modified in function, but not seriously altered in essence 
by its passage through the cow. The proteins constituting its mole- 
cules have not been changed, or, if at all, so slightly altered that one 
form still sensitizes to the other. The modified virus sensitizes the 
body cells and by this we mean that it causes the cell to elaborate a 
specific enzyme that digests and destroys the virus. The body cells 
retain this new function and when the smallpox virus finds its way 
into the body it is digested and destroyed before it has time to mul- 
tiply sufficiently to cause disease. This is the basis of all bacterial 
and protozoal vaccination. In securing his vaccine for chicken 
cholera Pasteur modified the organism by successive growths on 
artificial culture media. That for anthrax he obtained by growth 
at relatively high temperature and that for rabies by drying the 
cord. The vaccine for typhoid fever is obtained by the use of cul- 
tures killed by heat. All of these processes in the special instances 
modify the proteins of the organisms so slightly that they still sensi- 
tize to themselves. This is protein sensitization and gives protein 
immunity. It is wholly different from toxin action and toxin im- 
munity, and we should not confuse the two by discussing one in terms 


of the other. In protein immunity there is no antigen and no anti- 
body, and we will proceed more understanding! v if we stop employ- 
ing these terms in discussing protein sensitization. The toxins are 
either ferments or closely related bodies, and the substance that 
digests the protein on reinjection or in the sensitized state of the 
animal is a ferment and it is proper to speak of it as consisting of 
amboceptor and complement, but further than this the nomenclature 
introduced by the genius of Ehrlich to explain toxin action and 
reaction has no place in the literature of sensitization. 

If what has been stated be true, protein sensitization is a most im- 
portant factor in acquired immunity, and it will be well to discuss 
methods of using so powerful an agent in combatting disease. It 
should always be held in mind that any protein contains a powerful 
poison, and that no unbroken protein can be injected into the body 
without carrying with it this poison, and moreover, the parenteral 
digestion of a protein means that its poisonous group will be set free 
or activated in the body. The liberation of this poison occurs, not 
in the alimentary canal, the walls of which may protect the body or 
from which it may be rejected by vomiting or purging, or by both, 
but in the blood and tissue, and there is no escaping its effects. It 
is a poison, not a toxin, and there is up to the present time no known 
antidote for it. The indiscriminate employment of protein injec- 
tions now t being made should be most positively condemned. 

Work done in our own laboratory indicates that with some proteins 
at least the sensitizing and poisonous groups may be separated, and 
that when this is done the former sensitizes quite as efficiently and 
sometimes much better than the unbroken protein containing its 
poisonous group. In animals the nonpoisonous part of the typhoid 
protein gives immunity to the living bacillus to a much greater 
degree and more promptly than the unbroken bacillus, either alive 
or dead. It is freely soluble and the more soluble protein sensitizers 
are the more promptly and efficiently do they act. But the old idea 
that in order to protect a man against disease you must make him 
sick — and the sicker you make him the greater the protection you give 
him — is so strong in the profession that no one will listen to the use 
of a nonpoisonous split product to protect one against typhoid fever. 

That the tuberculous animal behaves quite differently from the 
nontuberculous on receiving injections of the tuberculin protein, 
whether it be in the form of the living bacillus, in dead cells, or in 
solution, has been abundantly demonstrated. Before Koch gave us 
tuberculin, Arloing and Courmont had come to the conclusion that 
the tubercle bacillus produces soluble substances which reduce the 
natural resistance of the body and render it more susceptible *to rein- 
fection. This corresponds closely with the first impression made by 
observation of the phenomena of anaphylaxis, the impression that 


led Kichet to select this term. In 1891 Koch described a perfect ex- 
ample of protein sensitization as we understand it to-day. He stated 
that when a healthy guinea pig is inoculated with the living tubercle 
bacillus there is no change at the site of inoculation until from 10 to 
14 days later, when a hard lump forms, finally opens and ulcerates, 
and continues until the animal dies. On the other hand, when a 
tuberculous guinea pig is inoculated with the living bacillus, on the 
second or third day a lump forms, soon becomes necrotic, falls out, 
ulcerates for a time, and finally heals without any infection of the 
neighboring lymph glands. In 1897 Trudeau observed that when 
healthy rabbits receive injections of virulent cultures in the eye, 
there is little to be seen for about 14 days, when with increasing 
vascularity tubercles form in the iris after which inflammation ex- 
tends and the eye is practically destroyed within from 6 to 8 weeks. 
Like treatment of tuberculous rabbits develops an iritis within from 
2 to 5 days, but at the end of the second or third week at a time when 
the controls begin to develop destructive changes, the inflammation 
begins to subside. Later studies have confirmed and amplified these, 
and it has been found that death may be induced within 24 hours by 
injecting a large amount of a living culture into a tuberculous 

The same difference between healthy and tuberculous animals has 
been observed in their response to injections of dead cultures of the 
tubercle bacillus. The first observation along this line, so far as we 
know, was made by Strauss and Gamaleia, who found that when 
large numbers of dead tubercle bacilli are injected into tuberculous 
animals death results while similar amounts are without immediate 
effect upon healthy animals. 

When we come to tuberculin, every phase of its action or its failure 
to act is explainable on the ground that the tuberculous animal is 
a sensitized one. Koch found that 0.5 gram of his preparation killed 
tuberculous guinea pigs, and induced no symptoms in healthy ones. 
A fraction of 1 milligram may cause marked symptoms in a tubercu- 
lous man, while many times this amount is borne easily by a healthy 
man. The inflammatory reaction about local tubercular lesions 
caused by injections of tuberculin is explained by the fact of the 
high degree of sensitization in their localities, and the cleavage of 
the bacilli. The ophthalmic, cutaneous, subcutaneous, and intra- 
venous tests with tuberculin are all typical sensitization reactions. 
Even in the failure to respond to tuberculin seen in advanced tuber- 
culosis we have the condition known as anti-anaphylaxis, which simply 
means that the anaphylactic ferment is exhausted by the large amount 
of material supplied by the bacilli in the body. 

There is another line of evidence that in tuberculosis there is a 
condition of specific protein sensitization. This is to be found in 


the fact that this disease is much more- deadly in lands and among 
people who have recently come under its influence than it is where it 
has prevailed for many generations. In other words, the widespread 
and long-continued existence of the disease, slowly, and at the cost 
of much sickness and many deaths, brings a certain degree of im- 
munity. The readiness with which the North American Indian has 
succumbed to this disease is a striking illustration, and Calmette has 
recently collected additional evidence on this point. He states that 
tuberculosis is being widely disseminated among peoples who have 
until recently been free from it. The world-wide wanderings of the 
white man are carrying the disease to every people, from the Lap- 
lander and Esquimaux of the arctics to the negroes and Malays of 
the tropics. Iceland, the Faro Islands, and the steppes of Russia are 
being infected and in these new regions tuberculosis exists in its 
most speedily fatal forms. The same author points out that recently 
discovered methods for the recognition of this disease even in latent 
states shows that among Europeans not more than 7 or 8 per cent 
reach more than 20 years of age without receiving the infection. 
Those who survive the first infection become more or less immune, 
and after that develop, when they do acquire the disease, the more 
chronic forms. 

Romer 5 concludes that the less widely is tuberculosis distributed 
among a people, the greater is the case mortality, and, the wider the 
distribution, the smaller is the case mortality. 

Still another fact of importance is that the most speedily fatal 
forms of tuberculosis, such as the miliary and meningeal, are much 
more frequent among children than among adults. 

There is another matter of much importance in this connection 
which we must discuss. We have found the tubercle bacillus highly 
resistant to lytic agents, and it appears that its long experience as a 
parasite has led it to protect itself with layers of wax and deposits 
of fat, but proteolytic enzymes digest the most firm proteins. Fried- 
berger has found that at least some strains of this bacillus are di- 
gested by the serum of healthy guinea pigs, and the researches of 
Merkl, Ba,il, and Kraus and his students have shown that tubercle 
baccilli placed in the peritoneal cavity of tuberculous animals respond 
to Pfeiffer's reaction. Some strains are dissolved in the peritoneum 
of healthy guinea pigs, but dissolution occurs more prompt^ and 
more completely in the peritoneum of a tuberculous animal. The 
healthy animal may have to depend upon its phagocytes to combat 
the invading bacillus, but the tuberculous animal supplies a specific 
proteolytic enzyme, and to this the fresh invader succumbs. 

Nature is slowly immunizing the white man to tuberculosis, and 
the question arises whether or not the process employed by nature 
can be aided in any way. We think it can, and there is not before 
66692— vol 2, pT 1—13 21 


the medical profession at this time a greater question than this, Is 
it possible to aid in eradicating tuberculosis by vaccination? What 
we need is a vaccine. Various methods of modifying the tubercle 
bacillus so that it could be used as a vaccine have been tried. The 
bovo-vaccine of von Behring was tried, but the increased resistance 
given by it was found to be of short duration. Attempts to reduce 
its virulence by age, heat, chemicals, and by submitting it to ultra- 
violet and other rays and emanations have been made. What we 
need is a tubercle protein sensitizer. It should be soluble and it 
should be free from the poisonous group in the protein molecule. 
In my opinion the nearest approach to this desired substance is the 
nonpoisonous portion of the tubercle protein, as prepared by the 
method of Vaughan and Wheeler. So far we have not been able 
to secure a uniform product. Some preparations seem to fill every 
requirement. They sensitize animals to the unbroken bacillus, dead 
or alive, and in surface tubercular lesions they cause inflammation 
about the tubercular area, and we have seen the tubercular tissue 
slough off and complete recovery result, but other preparations 
made from the same cellular substance by the same method seem 
inert. We have had similar difficulties with the sensitizing groups 
from other proteins. Some preparations from egg white sensitize 
to unbroken egg white, while others seem wholly without effect, and 
still all are prepared from the same material and in the same way. 
Evidently the sensitizing group in the protein molecule is a highly 
labile body and susceptible to influences which so far we have not 
been able to recognize. We have no difficulty in obtaining the 
poisonous group uniformly, but it is otherwise with the sensitizing 
body. Further work along this line is needed, and if an efficient 
and uniformly reliable sensitizer for the tubercular protein, free 
from the poisonous group, can be secured, all children should be 
vaccinated for tuberculosis, then, with protection against natural 
infection, the restriction of tuberculosis will be as completely under 
man's control as is that of smallpox. It should be clearly under- 
stood that the protection afforded by vaccination is relative and not 

The studies inaugurated by Wright have demonstrated that vac- 
cination is of service not only in prevention, but also in cure. Bac- 
teria and protozoa are particulate, and in many diseases they are 
confined to limited localities. As we have seen, sensitization may 
also be local. No body cell is sensitized against a foreign protein 
until the latter comes in contact with the former, and penetration of 
the body cell is probably essential to the most efficient sensitization. 
The microorganisms of acne are located in the cutaneous tissue ; and 
being particulate and not in solution, the area sensitized by them is 
small, if there be any sensitization at all. By vaccine therapy the 


area of sensitization is greatly extended and the amount of lytic agent 
formed and made available is greatly increased. This being in solu- 
tion and diffusible, digests and destroys the bacteria located in the 
skin. The same is true of the treatment of localized tuberculosis 
or of any other localized infectious disease. In vaccine therapy, as 
in vaccination, the great need is for soluble sensitizers free from 
poisonous content. When these are secured, and not until then, we 
may develop a vaccine therapy along scientific lines and expect to 
secure important results with it. 

There is another possible way in which sensitization may be of 
service in treatment. We refer to the use of specific enzymes. This 
method is now being tried by J. W. Vaughan in the treatment of 
cancer. He sensitizes rabbits or sheep to the cancer cell by injections 
of finely ground cancerous tissue or the nonpoisonous portion of the 
same. When the large mononuclear leucocytes reach 25 per cent or 
more he bleeds the animal, lakes the blood with acetic acid, and col- 
lects the leucocytes in a centrifuge. These are rubbed with sterile 
sand in salt solution and passed through a Berkefeld filter. The 
filtrate contains the specific proteolytic ferment which splits up 
cancer cells. This is shown by incubating it with cancer cells when 
the poisonous portion of the protein molecule is set free, as is shown 
by the fact that when injected into fresh rabbits it causes sudden 
death. Incubated with other proteins the leucocytic extract liberates 
no poison. This leucocyte extract when injected in certain amounts 
directly into cancerous tissue induces anaphylactic shock. The effect 
of injections of small doses in parts of the body more or less remote 
from the cancerous tissue is now being tried, but it is too early to 
determine the value of this kind of treatment. This work seems 
to indicate that the specific anaphylactic enzyme for cancer cells is 
furnished by the large mononuclear leucocytes. It might be asked, 
Why not use the serum of the sensitized animal? This is not pos- 
sible, for two reasons: (1) Repeated injections of the serum cause 
albuminuria, and (2) they sensitize to the proteins of the serum. 
When the leucocytic extract is filtered through a Berkefeld filter it 
does not sensitize to the blood protein ; when this step in the process 
is omitted it does so sensitize. In work of this kind lies a promise 
of at least partially isolating the anaphylactic enzymes and studying 
their effects. It is not probable that this treatment will ever prove 
practical for the removal of large areas of diseased tissue. 


It is interesting and instructive to read the older literature on fever 
in the light of the knowledge which has been gained in the study 
of sensitization. It has long been known that the parenteral intro- 
duction of proteins in small amounts, and especially repeated in- 


troduction, leads to fever. The older literature on this subject, as 
well as an account of his own work, was given in 1883 by Roques. 6 
In 1888 Gamaleia 7 showed quite clearly that fever accompanies and 
results from the parenteral digestion of bacterial proteins, and a year 
later Charrin and Buffer 8 confirmed this work and extended it to 
nonbacterial proteins. In 1890 Buchner 9 produced the characteristic 
phenomena of inflammation — color, rubor, tumor, and dolor — by the 
subcutaneous injection of diverse bacterial proteins. In 1895 Krehl 
and Matthes 10 induced fever by the parenteral introduction of albu- 
moses and peptons, but they did not obtain constant results, which 
we now know are secured only by regulation of the size and frequency 
of the dosage. In 1909 Vaughan, Wheeler, and Gidley 1X demon- 
strated that any desired form of fever — acute fatal, continued, inter- 
mittent, or remittent — can be induced in animals by regulating the 
size and frequency of the doses of foreign protein administered 
parenterally, and in 1911 Vaughan, Cumming, and Wright 12 ex- 
tended the details of this work. These investigators established the 
following points: 

(1) Large doses of unbroken protein administered intra-abdomi- 
nally, subcutaneously, or intravenously, have no effect upon the tem- 
perature ; at least, do not cause fever. 

(2) Small doses, especially when repeated, cause fever, the forms 
of which may be varied at will by changing the size and the interval 
of dosage. 

The following illustrations may be given : August 22, 1909, we in- 
jected the whites of three eggs into the abdominal cavity of a 
rabbit. The highest temperature of the fore period was 100.9°. 
After this injection the temperature was taken every two hours from 
8 a. m. to 6 p. m., up to September 6. The animal was weighed 
each day, and its urine measured and tested for albumin. There was 
no fever; indeed, the morning temperature fell some days to 97°, and 
one day to 96.6°. The animal lost in weight slightly more than one- 
fifth of its original. The volume of urine averaged normal, and at 
no time did it contain albumin. On the other hand 0.05 cubic centi- 
meters of egg white, filtered through cotton, injected intra-abdomi- 
nally every half hour from 8 a. m. to 4 p. m. carried the temperature 
to 106.6°. 

The intravenous injection of from 4 to 10 cubic centimeters of a 
dilution of egg white with an equal volume of salt solution every 
two hours from 8 a. m. to 6 p. m. had but little or no effect on the 
temperature, while the hourly injection of 1 cubic centimeter of the 
same solution and of much more dilute solutions carried the tempera- 
ture within from 4 to 6 hours up to from 105° to 107°, and in some 
instances caused sudden death. 

(3) The effect of protein injections on the temperature is more 
prompt and marked in sensitized than in fresh animals. 


(4) The intravenous injection of laked blood corpuscles from 
either man or the rabbit causes in the latter, even in very small 
quantity, either in single or repeated doses, prompt and marked ele- 
vation of temperature. 

(5) Laked corpuscles after removal of the stroma by filtration 
have a like effect. 

(6) Protein fever can be continued for weeks by repeated injec- 
tions, giving a curve which can not be distinguished from that of 
typhoid fever. 

(7) Protein fever is accompanied by increased nitrogen elimina- 
tion and gradual wasting. 

(8) Protein fever covers practically all cases of clinical fever. 

(9) Animals killed by experimentally induced fever may die at 
the height of the fever, but as a rule the temperature rapidly falls 
before death. 

(10) Fever induced by repeated injections of bacterial proteins 
and ending in recovery is followed by immunity. 

(11) The serum of animals in which protein fever has been in- 
duced digests the homologous protein in vitro. 

(12) Fever results from the parenteral digestion of proteins. 

(13) There are two kinds of parenteral proteolytic enzymes, one 
specific and the other nonspecific. 

(14) The production of the nonspecific ferment is easily and 
quickly stimulated. 

(15) The development of the specific ferment requires a longer 

(16) Sensitization and immunity are different manifestations of 
the same process. 

(17) Foreign, proteins, living or dead, formed or in solution, 
when introduced into the blood soon diffuse through the tissues 
and sensitize the cells. Different proteins have predilection places 
in which they are deposited and where they are, in large part at 
least, digested, thus giving rise to the characteristic symptoms and 
lesions of the different diseases. 

(18) The subnormal temperature which may occur in the course 
of a fever or at its termination is due to the rapid liberation of the 
protein poison, which in small doses causes an elevation, and in 
larger doses a depression, of temperature. 

(19) Fever per se must be regarded as a beneficent phenomenon 
inasmuch as it results from a process inaugurated by the body cells 
for the purpose of ridding the body of foreign substances. 

(20) The evident sources of excessive heat production in fever 
are the following: 

(a) That arising from the unusual activity of the cells supplying 
the enzvme. 


(b) That arising from the cleavage of the foreign protein. 

(c) That arising from the destructive reaction between the split 
products, from the foreign protein and proteins of the body. 

In 1910 Friedberger 13 studied the effects of graduated doses of 
foreign proteins on the temperature of both normal and sensitized 
animals. With lambs' serum intravenously administered to normal 
guinea pigs he obtained the following results : 

5.0 cubic centimeter equals fatal dose. 

0.5 cubic centimeter equals limit for fall in temperature. 

0.01 cubic centimeter equals upper constant. 

0.005 cubic centimeter equals fever plane. 

0.001 cubic centimeter equals lower constant. 

In sensitized guinea pigs the above figures were changed to the 
following : 

0.005 cubic centimeter equals fatal dose. 
0.0005 cubic centimeter equals limit for fall. 
0.00001 cubic centimeter equals upper constant. 
0.000005 cubic centimeter equals limit for fever. 
0.000001 cubic centimeter equals lower constant. 

In 1911 Schittenhelm, Weichardt, and Hartmann 14 experimented 
with the effect of the parenteral administration of diverse proteins 
on animal temperature and came to the following conclusion, which, 
in our opinion, is well stated : " In severe experimental anaphylaxis 
there is a fall in temperature; in the lighter manifestations there is 
fever." We regard this as a confirmation of our conclusion reached 
some years earlier. " Small, especially repeated, doses of the protein 
poison cause fever, while large doses depress the temperature." 

Some years ago Friedmann and Isaak 15 showed that after the 
parenteral introduction of foreign proteins the increase in nitrogen 
elimination is greater than can be accounted for by the protein 
injected. This has been confirmed by the work of Schittenhelm and 
Weichardt 16 and, as has been stated, Vaughan, Wheeler, and Gidley 
found the same in protein fever. Our explanation for the marked 
increase in nitrogen elimination has been given. 

In intermittent and remittent fevers and in relapses in all infec- 
tious diseases the phenomena of protein sensitization are fully 
demonstrated. In the different forms of malaria, chill and fever 
correspond to the discharge of foreign protein into the blood just 
as promptly as anaphylactic symptoms follow the injection of the 
homologous protein in a sensitized animal. The moment the blood 
cells rupture and the protozoal protein is disseminated the sensi- 
tized cells discharge the lytic ferment by which the foreign protein 
is disrupted and destroyed, but in this process the poison is liberated. 

Local sensitization is frequently established in the mucous mem- 
brane of the air passages and of the alimentary canal, also in the skin 


for two reasons. In the first place, foreign proteins are frequently 
brought into direct contact with these tissues, and in the second place, 
as has been shown in my laboratory, foreign proteins introduced into 
the blood are frequently deposited in the skin and in the walls of the 
alimentary canal. These local sensitizations characterize many of the 
infectious diseases. The work of Dunbar and Weichardt on hay 
fever is a nice illustration. These investigators injected each other 
subcutaneously with minute quantities of pollen suspension. Im- 
mediately Dunbar, being a hay-fever subject, became dizzy and within 
a few minutes began to sneeze, then a whoopinglike cough began. 
The eyes were congested, and an abundant secretion flowed from the 
nose. The face became swollen and cyanotic, and soon the body was 
covered with an urticarial rash. After 24 hours these symptoms sub- 
sided. Weichardt, not being a hay-fever subject, was not affected. 
That this and kindred affections are not benefited by antisera was 
abundantly and positively demonstrated by the failure of the so- 
called hay-fever serum, which was found in no instance to be of 
special value, and in some it greatly intensified the symptoms. 

Our common colds, or coryzas, are instances of local sensitization. 
Schittenhelm and Weichardt tell of a man who was so deeply sen- 
sitized by the inhalation of Witte's pepton that he could tell on enter- 
ing the laboratory- whether the pepton flask was open or closed, and 
some moist pepton painted on the skin caused the area covered to be- 
come red. The high degree of susceptibility to odors from the horse 
shown by some people has already been referred to. It seems in some 
instances that this susceptibility is transmitted from mother to child. 

In conclusion, I wish to state that all the problems of protein sensi- 
tization have not been solved. It seems to be a physiologic law that 
the specific ferments elaborated by living cells are determined by the 
proteins brought into contact with them, but as yet we know but little 
concerning these bodies which we call ferments. That they are labile 
chemical bodies resulting from intramolecular rearrangement in the 
protein molecules of the cell seems a plausible theory, but, at present, 
it is only a theory. We know but little of the action of these so- 
called ferments upon their homologous proteins. Our knowledge of 
the chemistry of protein sensitizers is exceedingly limited, and, as I 
have pointed out, it is highly desirable that work in this direction 
should be prosecuted with vigor, because we need sensitizers free from 
the poisonous group. Furthermore, there is the question, why small 
doses of protein induce fever while large doses have no such effect. 
At present we have no satisfactory answer to this question. If it 
could be conclusively demonstrated that the toxins are ferments, the 
subject of the etiology of disease would be greatly simplified. I have 
elsewhere 17 given my reasons for holding that the toxins are fer- 


ments, and in closing this paper I wish to formulate what I believe to 
be two biologic laws : 

(1) When the body cells find themselves in contact with, or per- 
meated by, foreign proteins, they elaborate specific ferments which 
digest and destroy the foreign proteins. 

(2) When body cells are attacked by destructive ferments, they 
elaborate antiferments, the function of which is to neutralize the fer- 
ments and thus protect the cells. 

1 Jour. Infectious Diseases, 4, 476, 1907. 

2 Die Serurnkrankheit, 1905. 

3 Klinische Studien fiber Vakzination u. Vakzinale Allergie, 1907. 

4 Archives of Internal Med., 7, 259, 283, 1911. 
5 Beitrage z. klinik d. Tubrk. 22, 301. 1912. 

8 Substances thermogenes, Paris, 1883. 

7 Ann. de l'Institut Pasteur, 12, 229. 

8 C. R. Soc. Biol. 1889, 63. 

9 Berl. k. W., 1890, 216. 

10 Arch. f. exp. Path. u. Pharm. 85, 232, 1895. 

11 Jour. Am. Med. Ass. Aug. 21, 1909. 

12 Z. f. I. 9, 458 ; Trans. Ass. Am. Physicians, 1911. 

13 Ber. k. W. No. 42, 1910. 

14 Z. f. exp. Path. u. Ther. 1911. 

15 Ibid., 1905, 1906, and 1908. 

16 Zentralblt. f. d. ges. Physiol, u. Pathol, d. Stoffwechsel, 1910. 

17 Trans. Ass. Am. Physicians, 1911. 


By Frederick P. Gay and G. Y. Rusk, from the Hearst Laboratory of Pathology 
and Bacteriology, University of California. 

Since the critical work of Knorr 1 on toxins it has been generally 
accepted that antibodies are formed, not by a simple inversion of 
antigens, but by a reaction on the part of the cells of the animal that 
has received the antigen. Correlatively, it has been assumed that cer- 
tain cells have a particular affinity for a given antigenic substance 
and are presumably specifically fitted to produce the corresponding 
antibody. Ehrlich's receptor hypothesis, while stating this assump- 
tion more concretely, has in no instance given direct proof that any 
particular type of cell gives rise to any given antibody. The experi- 
ment of Wassermann and Takaki 2 that demonstrated the apparent 
neutralization of tetanus toxin by brain substance is no longer re- 
garded as a proof of the nerve-cell origin of tetanus antitoxin. In- 
deed the work of Loewi and Meyer 3 would show that injection of 
the toxin into nervous tissue produces an increased susceptibility of 


the animal to tetanus toxin rather than an increased resistance. 
The fact that tetanus toxin disappears rapidly from the circulating 
blood of susceptible animals and may soon be demonstrated in the 
central nervous system would not, it would seem, prove conclusively 
that the toxin may not also have been fixed and neutralized by other 
body cells. At least it would seem necessary to assume that the 
cells responsible for the antitoxin formation must first fix the an- 
tigen. This proof of antigen fixation, indeed, constitutes one of the 
methods that have been employed in searching for the locus of an- 
tibody formation. The only other apparent method of determining 
antibody origin would seem to lie in the early demonstration of 
antibodies in given cell groups before they are demonstrable in the 
circulating blood. 

Very little information, therefore, on the site of antibody forma- 
tion has been gained from studies on toxin and antitoxin. Our 
information, inconclusive as it is, has been obtained from the work 
with other antibodies, and we would do well to consider first what 
data have been accumulated in respect to each of the antibody 
types in turn. 


Pfeiffer and Marx 4 inaugurated the first systematic attempts to 
discover the origin of lytic antibodies. Their work would seem to 
indicate very clearly that the protective antibodies directed against 
the cholera spirillum are elaborated in the leucopoietic organs, par- 
ticularly in the spleen, but to a less extent in the bone marrow, inas- 
much as extracts of these organs protect guinea pigs from infection 
before the blood serum does. Deutsch 5 essentially corroborated 
these findings with B. typhosus and Castellani 6 with B. dysenteriae. 
Levaditi's 7 conclusions from his work with the spirillum of hen 
septicemia were likewise corroborative, but his conclusions would 
not seem justified by the experimental evidence. These authors all 
agree that the spleen is not essential, as its removal at best but 
slightly inhibits antibody formation; the bone marrow and lymph 
nodes are secondarily concerned. 

A careful inspection of Levaditi's experiments would seem to point 
to the blood stream as a possible source of antibodies, although his 
conclusions are different. Several authors, however, have attempted 
to disprove experimentally the local or leucocytic origin of the bac- 
teriolysins. Thus Stenstrom 8 found that the injection of bacteria 
plus leucocytes led to less antibody production than the injection of 
bacteria alone. Pfeiffer and Marx found less antibodies in the 
ground leucocytes of immunized animals than in the plasma. 
Deutsch found the lysins were not present in peritoneal exudate and 


Paetsch 8 extended this finding so as to include both pleural and 
peritoneal exudates and the lining endothelia of these cavities. 

Violle's 10 injections into the gall bladder for the rapid production 
of antibodies indicate the possible function of the liver in this con- 
nection, which is emphasized more distinctly in work with other 


Metchnikoff 1X and Cantacuzene 12 originally suggested, on what 
would seem to be largely philosophical grounds, that the hemolysins 
may be formed by the leucocytes owing to the recognized phagocy- 
tosis of blood cells by the mononuclears. The output of " fixatives," 
according to Metchnikoff, varies directly with the degree of phago- 
cytosis. There is direct evidence that goes to prove, however, that 
these bodies are not formed in the blood stream. McGowan 13 
showed that no leucocytosis follows the injection of alien blood and 
Hektoen and Carlson 14 have shown by transfusion experiments that 
the antigenic properties of foreign blood cells disappear from the 
circulation within seven hours. 

Among the fixed tissues, the liver and spleen seem to have shared 
the honors as the possible sites of hemolysin formation. Leuck- 
hardt and Becht, 15 following the work of Hektoen and Carlson, 
found that the spleen alone of the organs in a dog that has received 
goat or rat corpuscles 24 hours previously has the property of im- 
munizing new animals. As a proof of the temporary location of the 
red blood cells that have been injected, this evidence is undoubted, 
although well recognized from other work ; as a proof of the spleen 
as the site of antibody formation it would seem to be negative. The 
statement by London 16 that splenectomy decreases the formation of 
hemolysins is categorically denied by Jakuschewitch. 17 Brezina 18 
found that a specific serum against the leucopoietic organs had no 
effect in disturbing hemolysin formation. Carrel and Ingebristen 19 
have produced hemolysins in the growing embryonic spleen. 

The evidence in favor of the liver as the site of hemolysin for- 
mation is more positive. Both Cantacuzene 12 and McGowan 13 have 
shown the function of Kupfers cells in the destruction of red blood 
corpuscles. Muller, 20 in an interesting paper, has apparently traced 
normal hemolysin formation to the liver and has even been able to 
stimulate its excretion in the liver suspended in Kinger's solution 
outside the body, by transfusing it with solutions containing iodine 
(iodipin). A further contribution to the stimulating effect of iodin 
compounds is given by Hektoen 21 who was able to increase the output 
of hemolytic sensitizers in dogs by injecting sodium iodoxybenzoate. 
Violles 10 method of producing antibodies by gall-bladder injection 
has already been referred to under bacteriolysins. 



Whereas the evidence for bacteriolysin formation seemed to favor 
formation in the spleen or liver, the evidence for the locus of origin 
of the bacterial agglutinins points distinctly to the blood stream. 
Thus the work of Deutsch, 6 Castellani, 6 Rath, 22 Weil and Braun, 23 
and Kraus and Schiffmann 24 all shows that the agglutinins appear 
in the blood serum before they are present in the extract of any 
organ. Although Gruber 25 originally suggested that the polymor- 
phonuclears form the agglutinins, no experimental evidence goes to 
prove this. The experiments of Achard and Bensaud, 28 Widal and 
Sicard, 27 of Paetsch, 9 and of Kraus and Schiffmann 24 all seem to 
disprove leucocytic or local origin. 

There is some evidence of agglutinin formation in the spleen 
offered by v. Emden, 28 Jatta, 29 and Girgoleff. 5 



In the case of precipitin formation, again the evidence seems 
divided. It is shown by two sets of observers (Petit and Carlson, 31 
Vaughan, Cumming, and McGlumphy 32 ) that soluble antigenic sub- 
stances like egg white or serum apparently disappear within a few 
hours from the circulating blood. This is shown by the impossi- 
bility of producing, in the one set of experiments, antibodies in 
another animal that is liberally transfused with such blood, and, 
on the other hand, by the failure to produce anaphylaxis in guinea 
pigs to the substance originally injected (egg white, Vaughan and 
collaborators). In apparent contradiction are the observations of 
several observers on the relation of leucocytosis to precipitin forma- 
tion. Thus both Cantacuzene 83 and Swerew 34 have noted a marked 
hyperleucocytosis preceded by an absolute decrease in polymor- 
phonuclears, which may reasonably be related to the liberation of 
precipitins. This observation fits in neatly with that of Hiss and 
Zinsser, 35 who obtained nonspecific bacterial precipitins from leuco- 
cytic extracts, and that of Stenstrom, 8 who found that hemologous 
leucocytes injected with the precipitinogen increases precipitin out- 
put. Kraus and Schiffmann 24 emphatically regard the blood as the 
source of precipitins, whereas Cantacuzene, in spite of his evidence 
in favor of the leucocytes, is inclined to trace precipitin formation 
to the spleen. 

The liver is by no means to be overlooked in discussing precipitin 
formation. The work of Manwaring, 36 of Nolf, 37 and of Balizot, 38 
on anaphylactic shock, would seem to point to the liver as the seat 
of action, and so, indirectly, owing to the relation that exists between 
anaphylaxis and precipitins, as a possible location of the latter 


It is evident from this brief survey of the literature that no general 
statement can be made on the locus of antibody formation in gen- 
eral. It may well be that each of the antibody types is produced 
in a different place or places. But even when we consider the pos- 
sible seat of origin of any particular class of antibodies, we are 
struck by the apparent confusion in the acquired data. In the case 
of any of them we may still say that the antibody may be formed 
either in the blood stream or in the fixed tissues. There seems 
greatest agreement on the point that antibodies are formed either 
by the leucocytes or the leucocyte-forming organs. And yet a good 
deal of recent work points with increasing emphasis to the liver, an 
organ which, in view of its other functions, might logically likewise 
serve to produce antibodies. 

Our own studies on antibody formation have been actively in 
progress for over a year. We regard them hitherto as largely pre- 
liminary and they have led rather toward establishing certain meth- 
ods of attack and the evolution of working hypotheses of possible 
heuristic value than to any conclusion on the main subject at issue. 
Certain by-products of the investigation are in themselves of distinct 
interest, although their results are negative in so far as explaining 
antibody formation is concerned. Two incidental investigations 
may first be summarized before dealing with the work that bears 
more directly on the site of antibody formation : 


Muller's 20 experiments led him to the conclusion that both nor- 
mal sensitizer (amboceptor) and alexin are formed in the liver, 
but that their output depends on the stimulating action of the 
iodin of the thyroid gland. This author finds that the injection of 
thyroid preparations, or of various iodine preparations, notably of 
iodipin (Merck, 25 or 10 per cent of iodin), produces a distinct 
increase in from 24 to 36 hours of the normal hemolysins in rab- 
bits and other animals. As already stated, this increase comprises 
not only an increase in alexin, as tested on blood cells sensitized by 
an artificial hemolysin, but an increase of the normal hemolytic 
sensitizer. Hektoen 21 has further found an increase in hemolytic 
sensitizers in dogs that received a single dose of goat's blood over 
the amount produced in control dogs on giving injections of sodium 
iodoxybenzoate. This alleged increase of normal hemolytic sensi- 
tizers immediately suggested the importance of determining the 
effect of iodin on artificial hemolysins, not only as a matter in itself 
of theoretical and perhaps of practical importance, but as bearing 
on the origin of antibody formation. Differences that might appear 
in the hemolytic potency of the sera of immunized animals would 


presumably be more striking than corresponding differences in nor- 
mal hemolysins, owing to the much greater strength oi immune sera. 
Our experiments deal, first, with the effect of a single injection of 
iodipin (Merck, 10 per cent) in rabbits that had been immunized by 
several injections of washed guinea-pig corpuscles. In several ex- 
periments a control animal that had been immunized in a similar 
manner, but that received no iodipin, was carried through. The 
animals with and without iodipin were bled before injection from the 
ear and at intervals subsequently; the separate sera were heated at 
once to 56° for one-half hour, and at the end of the experiment all 
were tested for hemolytic units at the same time with the same cor- 
puscles and alexin. In other experiments a critical intravenous re- 
injection of the antigenic blood was given in two highly immunized 
rabbits, and on the following day one of them was given iodipin. 
Both sera were then tested at intervals for hemolytic potency. There 
was no evidence from any of these experiments that the injection of 
iodipin will increase the output of artificial hemolysins in the im- 
munized rabbits. 

GEN. 40 

The histopathological studies of Gay and Southard 41 in serum 
anaphylaxis in the guinea pig have seemed an interesting contribu- 
tion to the relation of structure to function. These authors found 
that anaphylactic intoxication is accompanied by definite lesions in 
the nature of hemorrhages and more particularly by fatty changes 
in parenchyma and in the endothelium. These endothelial fat 
changes could be produced in a few minutes following intravenous 
injection and obviously bear direct relation to the cyclonic symptoms 
of the syndrome. It occurred to us that similar evidence of func- 
tional cellular activity might be histologically demonstrable in the 
cells that are engaged in antibody formation. For this purpose 
rabbits were highly immunized by repeated intravenous injection of 
washed guinea-pig corpuscles and following a rest of two or more 
weeks were given a critical reinjection of 1 cubic centimeter of 
washed guinea-pig blood and at subsequent intervals bled and the 
tissues fixed in various ways and stained by many methods. The 
critical reinjection was aimed, obviously, to obtain the antibody- 
producing cells in a condition of highest activity. 

In the first experiment a series of immunized rabbits received 
each the critical reinjection of antigen and were then bled at 1, 4, 
and 24 hours and 4 and 6 days subsequently. A careful histological 
study of tissues from this series showed in the 24-hour animal a very 


marked increase of glycogen in the liver (Best's carmine stain, alco- 
hol fixation). The animals bled before and after this period gave 
a regular increase and decrease of glycogen to the 24-hour maximum. 
A more careful control of this experiment has involved us in techni- 
cal difficulties that seemed too time consuming and led, moreover, to 
far less encouraging results than the first experiment. The question 
of the effect of starvation on the amount of glycogen alone seemed 
unsurmountable ; it was found, for example, that rabbits that have 
not been fed for two days have stomachs stuffed with food. We are 
still in doubt as to the significance of our first find of increased 
glycogen. An attempt to correlate the microchemical reaction of 
glycogen with a careful chemical analysis of total glycogen in the 
liver has, however, led to results of importance. So far as we are 
aware, there has been no systematic comparison between the chemical 
analysis of an organ and microchemical staining reactions in a sam- 
ple of it. Dr. Rusk has studied the amount and distribution of 
glycogen in sections of 22 rabbit livers stained by the Ehrlich iodin 
method and the Best carmine method, with a chemical analysis of a 
greater (weighed) portion of the same livers, following Pfluger's 
method to the conversion of glycogen to glucose, and at this point 
introducing Betrand's modification of Fehling's method as more 
accurate in measuring the amount of copper reduced. It is found 
that the microchemical method serves to give somewhat definite in- 
formation as to the amount of glycogen present, but within a limited 
range only, for when the chemical analysis showed very much or 
very little glycogen the staining method was at times wholly 



The two general methods that have been and may be employed in 
seeking antibody origin are either to trace the course of the injected 
antigen to some group of cells or to seek the precocious appearance 
of antibodies in extracts of a given group of cells. The latter method 
is the one that has been used most frequently, but it is the former 
that we have employed. Our observations, some of which have 
already been published, 42 began with a study of the fate of horse 
serum injected into the blood stream of rabbits that had been im- 
munized against horse serum. They have since led to further studies 
on the result of an initial injection of horse serum in normal rabbits. 
In all instances our results deal with an injection of one cubic centi- 
meter of serum intravenously. 

In beginning the experiments with immunized animals it was neces- 
sary first to determine the best method of detecting the antigen that 


was reinjected. It was found that when horse serum is injected intra- 
venously in rabbits that have a high precipitin content for horse serum 
it nevertheless remains demonstrable by the fixation reaction or the 
precipitin reaction for 24 hours. The reactions are carried out by 
adding the antigen-containing antiserum to a pure antiserum. After 
48 hours the antigen is no longer demonstrable. The persistence of 
the antigen in the immune animal is accompanied by a fall in the 
precipitin value of serum (negative phase). It is of interest to note 
that although this antigen-containing antiserum will not precipitate 
or fix alexin spontaneously, it will react with another antigenic anti- 
serum as well as with a pure antiserum. It was rather surprising to 
us to fail in any conclusive demonstration of the antigen by the 
fixation reaction in extracts of the organs of these same immunized 
animals (spleen, lymph nodes, liver, kidney, and muscles) either 
at the same time the antigen is present in the blood or even 24 hours 

Of undoubtedly greater significance is the fact that neither the 
antigen-containing antiserum, nor the organ extracts of the same 
animal will sensitize guinea pigs to subsequent intoxication by horse 
serum. We compared the fixing values of pure horse serum and 
antigenic antiserum, and although one fixing dose of the horse serum 
will sensitize guinea pigs, many fixing doses of the antigenic anti- 
serum fail to do so (at least 100). This would explain the results 
of Vaughan, Cumming, and McGlumphy 32 who found that egg 
white apparently disappears from the circulation in a few hours 
when tested for by the anaphylaxis reaction. It is perhaps also in 
harmony with the work of Hektoen and Carlson 14 and of Petit 
and Carlson 31 who proved by transfusion that the antibody-incit- 
ing factor in blood cells or in serum leaves the circulation in a few 
hours. We might possibly assume that the factor in the antigen that 
produces the antibody differs from the one that unites with it. (Cfr. 
Bang and Forsmann. 43 

The results of injecting horse serum into normal animals are also 
of interest. The horse serum is detectable by the precipitin and 
fixation reactions for several days. It apparently does not sensitize 
in large doses even after 24 hours. The fixation and precipitinogen 
antigen is present not only in the blood, but also in the various organ 
extracts (in this case carefully freed of blood) in uniform amounts 
on the seventh, eighth, ninth, and tenth day. Of greatest importance 
is the fact that the corresponding antibodies have begun to appear 
in the serum two or three days before the antigen disappears. Simi- 
lar facts have been noted by Hintze. 44 It is evident then that not 
all the antigen is used up in producing the antibody. We have to 
imagine either that the antigen continues to unite with the cell or 


stimulate the cell for some time after antibodies appear, or that the 
antibody stimulant differs from the antigen fraction that unites with 
the antibody. This latter hypothesis seems to us for the present 
the most valuable for a working basis. It explains, moreover, our 
own failure to produce anaphylaxis (cfr. also Vaughan and his 
collaborators), and also the results of Hektoen and Carlson. We are 
continuing our work with this as a working hypothesis and also 
with a possible further elucidation of the obscure phenomenon of 
anaphylaxis in mind. 

^vnorr: Fortsehr. der Mediz., etc., vol. 15 (1897), p. 657. 
'Wassermann and Takaki : Berlin. Klin. Woehen., vol. 35 (1898), p. 5. 
8 Loevvi and Meyer; Archiv fur experiment. Path., vol. 59 (1908), p. 355. 
*Pfeiffer and Marx: Zeit fur Hygiene, vol. 27 (1898), p. 272. 
5 Deutsch: Annates de l'Inst. Pasteur, vol. 13 (1899), p. 689. 
8 Castellani : Zeit. fiir Hygiene, vol. 37 (1901), p. 381. 
7 Levaditi: Annales de l'lust. Pasteur, vol. 18 (1904), p. 511. 
"Stenstrom: Zeit. far Irmnimitatsforsch., vol. 8 (1911), p. 483. 
•Paetsch: Centralblatt fiir Bakt, Orig. I, vol. 60 (1911), p. 255, 
10 Vio!le: Annales de l'Inst. Pasteur, vol. 26 (1912), pp. 381, 467. 

11 Metchnikoff : L'immunite dans les maladies infectieuses, p. 103; Annales 
de l'Inst. Pasteur, vol. 13 (1899), p. 737. 

12 Camyicuzene : Annales de l'Inst. Pasteur, vol. 16 (1902), p. 522. 

13 McGowan : Journal of Pathology and Basteriology, vol. 14 (1909), 379; 
vol. 15 (1911), 262. 

"Hektoen and Carlson: Transact. Chicago Path. Soc, vol. S (1909), p. 4; 
Journ. of Infect. Diseases, vol. 7 (1910), p. 319. 
15 Leuckhardt and Becht: Transact. Chicago Path. Soc, vol. 8 (1911), p. 202. 
16 London: Archie fiir biologische Wissenschaften (1901), p. 328. 
17 Jakuschewitsch : Zeit. fiir Hygiene, vol. 47 (1904), p. 407. 
18 Brezina: Wein. Klin Wochenschr. (1905), p. 905. 
"Carrel and Ingebristen: Journ A. M. A., vol. 58 (1911), p. 477. 
20 Muller: Central, fiir Bakt, I. Abt, Orig., vol. 57 (1911), p. 577. 

21 Hektoen: Transact. Chicago Path. Soc, vol. 8 (1911), p. 138. 
22 Rath: Central, fur Bakt, vol. 25 (1899), 529 

23 Weil and Braim: Biochem. Zeitschr., vol. 17 (1910), p. 337. 

M Kraus and Schiffman: Annales de l'Inst Pasteur, vol. 20 (1906), 225. 

•Gtttber: Munch, mediz. Wochenschr. (1S97), Nos. 17 and 18. 

*Achard and Bensaud: Archiv fiir med. Experiment (1896), p. 748. 

27 Widal and Sicard : Annales de l'Inst. Pasteur, vol 11 (1897), p. 353. 

28 v. Emden: Zeit. fur Hygiene, vol. 30 (1899), p. 19. 

28 Jatta: Zeit. fur Hygiene, vol. 33 (1900), p. 185. 

S0 Girgoleff : Zeit. fiir Immuitatsforch., vol. 12 (1912), p. 401. 

81 Petit and Carlson: Jour. Infect. Diseases, vol. 10 (1912), p. 43. 

22 Vaughan, Cumming & McGlumphy: Zeit. fiir Immunitatsforsch., vol. 9 
(1911), p. 16. 

33 Cantacuzene : Annales de l'Inst Pasteur, vol. 22 (1908), p. 54. 
"Swerew: Russky Wratsch. (1910) , p. 367; Ref. Jahresbericht der Immuni- 
tiitsforschung, VI 2 , p. 527. 


35. Hiss and Zinsser: Jour. Med. Research, vol. 19 (1908), p. 399. 
3G. Manwaring: Zeitschr. fiir Immunit&tsforsch., vol. 8 (1910), p. 1. 

37. Nolf : Archives iuternat. de Physiolog., Vol. X (1910), p. 37. 

38. Blaizot: Compt. rend. heb. Soc. de Biol., vol. 70 (1911), p. 383. 

39. Gay & Rusk: Univ. Calif. Publ. Path., vol. 2, No. 7 (1912). 

40. Rusk: Univ. Calif. Publ. Path., vol. 2, No. 9 (1912). 

41. Gay and Southard: Jour. med. Research, vol. 16 (1907), p. 143. 

42. Gay and Rusk: Univ. Calif. Publ. Path., vol. 2, No. <; M912). 

43. Bang and Forssmann : Centralblatt fur Bakt., I. Orig., XL (1905), p. 151. 

44. Hintze: Zeit. fiir Immunitatsforsch., vol. 6 (1910), p. 113. 



Dr. W. H. Park : Observations made on the injection of toxins and 
antigens into the blood or into the subcutaneous or other tissues in- 
dicate that for many antibodies several varieties of cells take part. 
The blood in an animal highly immunized to diphtheria toxin contains 
about 100 times the quantity of antitoxin as the tissue fluids. If toxin 
is added to antitoxin, union slowly takes place and the combined toxin 
is no longer able to excite the production of antitoxin. When a horse 
having a strongly antitoxic blood is injected intravenously with a 
definite amount of toxin very little production of antitoxin takes 
place, because most of it is neutralized by the antitoxin in the blood. 
The same amount injected in scattered spots subcutaneously will 
produce a large amount of antitoxin. The part absorbed into the 
blood would meet the same fate as that injected intravenously. It 
seems, therefore, certain that some or all of the cells in the area in the 
subcutaneous tissues that the toxin reaches must take part in pro- 
ducing antitoxin. If toxin is injected through the trachea into the 
lungs it acts in the same way as when injected subcutaneously. I 
have seen similar, though not as definite, results with the injection 
of various bacterial antigens. These facts seem to suggest that 
more varied cells than Dr. Gay indicates may take part in antibody 

Dr. Vaughn thinks that the ferment is formed by different cells 
according to the sensitizer used. He referred to the work of J. W. 
Vaughan on sensitization to cancer proteins in which it appears 
that the ferment is formed in the large mononuclear leucocytes and 
that the sensitization is transitory. The fact that the nonpoisonous 
part sensitizes may be due to the presence of a minute trace of un- 
broken proteins. However, this seems highly improbable because 
this part does not sensitize to itself. 

66692— vol 2. ft 1—13 22 



Dr. E. C. Rosenow, of the Memorial Institute for Infectious Diseases, Chicago. 

I wish to present here very briefly the results of experiments which 
it is believed throw some light upon the nature of intoxication in 
pneumococcus anaphylaxis and in pneumococcus infections. It is 
obviously impossible to give details or to discuss the various investi- 
gations which bear directly or indirectly upon results obtained. For 
these, reference must be made to the more complete papers published 
chiefly in the Journal of Infectious Diseases during the past few 

•When normal animals, guinea pigs and dogs, are injected intra- 
venously with dead pneumococci or unautolysed extracts of pneumo- 
cocci, they die in from 6 to 24 hours, depending upon the dose. Sen- 
sitized animals die at a relatively earlier period in both instances, 
and, in case of the extract, from typical symptoms of anaphylaxis. 

When virulent pneumococci are suspended in NaCl solution, espe- 
cially if ether is added; when unautolysed pneumococcus extracts 
or pneumococci are treated with immune serum, or with normal 
serum alone, or with a combination of these, there appears in solu- 
tion, at a certain period, toxic material which kills guinea pigs and 
dogs with symptoms characteristic of anaphylaxis for each species. 
During the height of the toxicity for normal animals the mixtures 
containing the clear extracts have already lost a large part of their 
toxicity for the sensitized animals, and, finally, after longer resi- 
dence at 37° C, the toxic action disappears both for normal and 
sensitized guinea pigs and dogs. 

The toxic material obtained from pneumococci in vitro and in the 
sensitized animals does noi differ essentially from that formed dur- 
ing pneumococcus infections, because the same type of toxic material 
is found in solution in various pneumococcus exudates, and because, 
after these are washed and again suspended, in NaCl solution at 
37 ° C., more toxic material is formed in vitro and also, in an hour or 
more, following immediate injection into normal animals. When ex- 
tracts of pneumococcus exudates are kept at 37° C. for a longer time, 
both the immediate and late toxic action disappears, just as in the 
case of the extracts, in NaCl solution, of artificially grown pneumo- 
cocci. The pneumococci in the various mixtures which yield the toxic 
substance tend to become Gram negative and undergo disintegration. 
This is most marked in the extracts in NaCl solution. Only highly 
virulent pneumococci which contain an autolytic ferment, and which 
disintegrate rather rapidly, yield the highly toxic substance. Non- 
virulent pneumococci and occasional virulent strains which either do 
not autolyse at all, or only very slowly, do not yield the toxic sub- 


stance when suspended in NaCl solution. They do yield it, however, 
when treated with immune and then with normal serum, or with nor- 
mal serum only; but, in each case, more slowly than highly virulent 
strains. The toxicity of the pneumococci disappears as they dis- 
integrate and become Gram negative, and then no toxic substance can 
be obtained even when treated with fresh serum. The appearance 
and disappearance of the toxic substance, when virulent pneumococci 
are suspended in NaCl solution, has been proved to be associated with 
proteolysis. Proteolysis does not occur in case of nonvirulent pneu- 
mococci. When unautolysed, heated (60° C. one hour) pneumococcus 
extracts are treated side by side with sensitized and normal serum, it 
is found that the mixture in sensitive serum becomes toxic at an 
earlier period than that in normal serum, and it also disappears cor- 
respondingly earlier. Polariscopic measurements, made at the same 
time, show a more rapid decrease in levorotation in the former, indi- 
cating that here too the appearance and disappearance of the toxic 
substance occurs simultaneously with proteolysis. 

By grinding pneumococci in the cold I have been able to show that 
little toxic material is preformed within them. The extracts ob- 
tained in this way, when injected at once, produce no immediate 
symptoms, but death within 24 hours; after they are kept at 37° C. 
for a time, they cause death in a few moments; and, still later, they 
produce neither immediate nor late symptoms. It seems certain, 
therefore, that mature pneumococci contain little preformed toxic 
matter, but yield a large amount as they disintegrate, both in vitro 
and in vivo, and it makes no essential difference whether they are 
grown artificially or in the infected host. 

A comparative study of the toxicity of meat broth, and the cor- 
responding clear culture ; fluid or filtrate, shows that the latter is 
strikingly more toxic than the former. This has been shown not to 
be due to increase in acidity. Formol titration shows a correspond- 
ing increase in amino nitrogen. The exact source of the toxic 
material in this case is not entirely clear. I have pointed out that 
extracts of virulent pneumococci, in distinction to those of nonviru- 
lent pneumococci, liberate a proteolytic enzyme. In order to deter- 
mine whether this or other ferments obtainable from virulent pneu- 
mococci may produce similar toxic material from protein other than 
that contained in pneumococci, and at the same time produce protein 
cleavage, diminishing amounts of broth culture filtrates and filtered 
extracts in NaCl solution were added to meat broth and heated 
ascites meat broth, and placed at 37° C. It was found that both 
the broth culture filtrate and NaCl solution extract cause an increase 
in toxicity and amino nitrogen. Neither of these could possibly 
have had their origin in the small quantity of culture filtrates or 
extracts which were added. Hence a proteolytic enzyme escapes 


from virulent pneumococci, which is responsible for part of the pro- 
tein splitting, and the increase in toxicity when pneumocacci are cul- 
tivated in broth. A portion of the protein splitting, on the other 
hand, is intimately associated with the growth of the pneumococci. 
This is probably independent of the soluble ferment, because growth 
of nonvirulent pneumococci and streptococci, from which no soluble 
proteolytic enzyme can be obtained, causes both a splitting and an 
increase in toxicity when cultivated in broth. 

The relation of protein splitting to the production of toxic sub- 
stances is further shown by the following facts : The increase in tox- 
icity in the mixtures of meat broth and culture filtrates and extracts 
is proportionate to the amount of protein splitting up to a certain 
point; after that, the toxicity diminishes and the splitting increases. 
In the broth cultures from which the pneumococci are not removed, 
whether killed by adding ether or not, the late diminution in toxicity 
is not observed. In this connection, the following interesting facts 
should be mentioned: The proteolytic enzyme is more resistant to 
heat and long standing in the broth culture filtrates than in the NaCl 
solution extracts. The toxic effect of clear pneumococcus extracts 
disappears promptly when heated to 60° C., whereas, in the NaCl 
solution suspensions, in which a rather large number of unautolysed 
pneumococci are still present, heating to 60° C., and even boiling for 
10 minutes, often diminishes the toxicity only slightly. The toxicity 
now remains indefinitely on standing. This is especially true when 
the suspension is plunged at once into boiling water. In a similar 
manner the clear broth culture filtrates lose their toxicity more 
readily than the broth culture fluids from which the pneumococci 
are not removed, but not as readily as the clear extracts. Finally, 
when pneumococcus broth cultures, to which ether has been added, 
are kept at 37° C. for a long time and then filtered, and the proteoly- 
tic enzyme is no longer active, then heating the clear filtrate no 
longer diminishes the toxicity. From these facts, it appears that 
the toxic substance is really a stable compound, and that its disap- 
pearance from the mixtures is due to ferment action. Hence its 
disappearance on heating the clear extracts when the supply of ma- 
terial from which more toxic substance is made is limited, and its 
persistence in the suspensions when the supply is abundant. 

Protein splitting is undoubtedly a factor in the production of the 
toxic substance ; but that it is not the only factor is indicated by the 
fact that occasionally no perceptible increase in amino nitrogen is 
found in mixtures which are nontoxic at first, very toxic later, and 
again nontoxic still later. 

From these facts it would appear then that there are three more or 
less independent sources of toxic material during pneumococcus 
infections, each one of which is closely related to protein cleavage. 


They are (1) the pneumococci themselves (structural nitrogen) ; (2) 
growth in fluids or exudates (metabolic nitrogen) ; and (3) the 
action of the proteolytic enzyme on protein derivatives other than 
those from pneumococci. Certain facts indicate that other enzymes 
probably also play a role in the production and destruction of the 
toxic substances. 

A study of the action of the toxic substances obtainable from pneu- 
mococci shows that the various drugs and procedures which protect 
sensitized guinea pigs against immediate anaphylaxis protect normal 
guinea pigs against the toxic substance. Injections in the jugular 
vein or right heart produce severer symptoms than injections in the 
left heart. Portal injections in well-fed guinea pigs produce little or 
no pulmonary symptoms ; whereas, in starved animals, the symptoms 
are as marked as after jugular injections. 

The toxic substance is soluble in ether. Guinea pigs which are 
injected a short time previously (2 to 24 hours) with nonfatal doses 
of toxic extracts, and especially of the extracts from which the 
toxicity has disappeared, are protected against fatal doses of extracts. 
This seems specific for pneumococcus products, because injections of 
Nad solution, broth, and extracts of typhoid bacilli do not render 
guinea pigs refractory to toxic pneumococcus autolysates. After it 
was found that the toxic substance was soluble in ether, the protec- 
tive effect of the extracts after ether extraction, and of the ether 
soluble portion, was tested. The former afforded protection, while 
the latter did not. It has been found further that the nontoxic 
extract affords protection in the guinea pig against properly gauged 
doses of virulent pneumococci, whereas the toxic substance hastens 

Dead pneumococci and pneumococcus extracts, when injected in 
man, produce an increase in opsonin after an initial negative phase, 
while autolysed pneumococci, which have lost their toxic action, 
cause a more prompt rise in opsonin. By injecting proper doses of 
a combination of the toxic autolysates and autolysed pneumococci, I 
have been able to produce a continued negative phase similar to that 
observed in overwhelming pneumococcus infections. The mechanism 
of immunity seems paralyzed. 

It is generally held that intoxication and immunization are due to 
the same cause. The above results indicate strongly, as also do cer- 
tain clinical facts, that, in pneumococcus infections, at least, this 
seems not to be so, but that here there are produced substances which 
intoxicate, but which do not call forth protective reactions, and which 
probably actually interfere w T ith antibody formation. 


Dr. L. W. Famulener, Research Laboratory, Department of Health, New- 
York City. 

Over a century ago Huf eland * suggested that the milk excreted by 
a mother who had recovered from smallpox might exert a protective 
power over the nursing infant. He based this supposition upon the 
infrequency of smallpox among infants during the first months after 
birth. It is noteworthy that the theoretical explanation which he 
suggested took in account hypothetical antipoisons which roughly 
corresponded to our present idea of antitoxins or immune bodies. 

Many years later the isolation and successful cultivation of specific 
organisms causing various infectious diseases was accomplished and 
methods of animal immunization were developed. Experimental 
studies showed, in some instances, that animals which had been pre- 
viously immunized gave birth to young which were also immune to 
the specific infectious agent. This was commonly supposed to be 
an inherited immunity on the part of the offspring. In 1892 Ehrlich 
published his basic studies upon this subject. By those well-known 
experiments in which he immunized mice by feeding the toxalbumins, 
abrin and ricin, he showed that the young from such mothers were 
immune. He considered this a passive immunity and not a true 
inherited condition. The offspring in those cases acquired their anti- 
bodies in part before birth from the mothers' circulating fluids 
and in part after birth from the mothers' milk. He proved by placing 
normal young upon immune nurses that the milk transmitted specific 
antibodies which were absorbed unchanged by the nurslings and 
caused their immunization. Those studies firmly established the 
important role which the milk of immunized mothers may play in 
transmitting immunity to the offspring. It was soon found by 
Ehrlich and his coworkers that other animals, such as goats, when 
immunized against tetanus or diphtheria during the period of lacta- 
tion excreted the respective antitoxins with the milk; the amount of 
antitoxins in the milk increased as the content in the animal's serum 

Since those early studies numerous investigations have been re- 
ported along similar lines, which show that the milk of highly 
immunized animals may contain any of the common types of anti- 
bodies; the presence of antitoxins, specific agglutinins, cytolysins, 
precipitins, etc., have been demonstrated in the milk of immunized 
animals. In some instances their transmission and absorption in an 
unchanged condition have been proved in the blood serum of the 
nursing young. We may accept as an established fact that anti- 
body-bearing milk is an important factor, under certain restricted 


conditions, in the transmission of immunity to the nursing young. 
This ability depends much upon the antibody concentration of the 
milk; the age of the recipient is also an important factor. In 
general, the newly born animal quite readily absorbs antibodies in 
an unchanged condition. As a general thing, animals actively im- 
munized during the period of lactation do not show an antibody 
concentration of the milk, as compared to the blood serum, greater 
than one-twentieth of the serum value. The relative values are 
usually much less, probably depending in part upon the antigens 
used for immunizing purposes. Further, under such circumstances 
the increase in age of the offspring precludes the absorption of the 
antibody of the milk in an unchanged condition when taken as food. 
Experimental evidence would indicate that the most favorable 
condition for the transmission of immunity from the mother to the 
offspring through the milk exists at the time of the birth of the 
young. This, naturally, means that the mother must be immunized 
some time previously in order that milk from the first may bear suffi- 
cient quantity of the specific substances. Since we have had an 
opportunity to carry out certain experiments along this line, a brief 
report of the results may prove to be of interest. Immunizations 
were carried out upon female goats, by repeated subcutaneous in- 
jections of washed sheep-blood cells, at different periods before the 
birth of the young. In order to prevent the young from taking the 
colostrum at birth before samples of their blood were secured, the 
adult's nipples were previously sealed with collodion. As soon as 
possible after the birth of the young, a blood sample was taken from 
the kid ; then the seals were removed from the mother's nipples and 
a sample of colostrum taken ; finally a blood sample was taken from 
the adult. Immediately after the first blood sample was drawn from 
the newly born animal and the colostrum sample taken from the 
mother, the young was permitted to suckle and remain with the 
mother from that time onward. Both blood and milk samples w T ere 
taken from the mother and blood samples from the suckling at 
intervals for some time following the period of birth. The assembled 
samples, which had been kept in the ice box, were all tested at the 
same time in parallel, thus giving comparable results. In some in- 
stances the colostrum was found to contain more specific antibodies 
than the mother's serum did at time of birth of the young. Usually 
in those cases the immunization had been carried out several weeks 
previously, and the serum antibodies had greatly diminished in 
quantity. The antibody content of the colostrum milk rapidly di- 
minished as the milk excretion set in and was usually negative after 
a few days. In case of twins, one was removed from the mother, a 
blood sample taken, and then placed upon cow's milk as a control. 
Samples of blood taken from kids at time of birth (before being 


permitted to suckle mother) and those from the kid which was fed 
cow's milk never showed the presence of haemolysins by the test 
used. Therefore we must conclude that little, if any, passed from the 
mother-animal's circulation to the young before their birth. The 
kids which were permitted to suckle the immunized mother, thus 
getting the colostrum milk, showed considerable amount of the 
specific immune body in their blood serum on the first day following 
birth. Rarely did this content rise on the second day. Following 
this, the antibody content of the kids' blood gradually fell, similar to 
the ordinary passive immunity curve of the animal thus immunized. 
If we are permitted to draw conclusions from this series of ex- 
periments, it becomes evident that the complex cytolytic antibody 
formed in response to blood-cell injections readily passes over (in an 
unchanged condition) to the blood of newly born suckling from the 
ingested colostrum of the previously immunized mother. But little, 
if any, passes over from the immunized mother's body fluids to the 
offspring before their birth. These experiments would indicate that 
the antibodies resulting from immunization of females before birth 
of the young tend to accumulate in the mammary glands and are 
excreted with the colostrum milk. The question arises, Do the natu- 
ral antibodies likewise accumulate in the milk glands of normal 
mothers? If so, does the colostrum play a more or less important 
part by transmitting natural protective substances from the mother 
to the child? Is the transient resistance which infants commonly 
show against certain infections during the first weeks of .life in part 
acquired in this way? Certain experimental evidence along these 
lines would lend support to such a supposition. This may partially 
account for some of the advantages which the breast-fed child enjoys 
over the bottle-fed infant in the struggle against disease. 

1 Cited by Neumann, Deutsche nied. Wchnschr., 1895, 21 (part 2), p. 841. 


By Mr. Guido Volpino, charged with the course of bacteriology (with the col- 
laboration of Drs. A. Mariani, E. F. Bordoni, and L. Alpago Novello). 

1. The pellagra patients, when subjected to an inoculation of a cer- 
tain quantity of watery extract of spoiled maize, either undercutaneous 
or into the muscular masses, which are insufficient to produce appreci- 
able phenomena in the great majority of nonafflicted with pellagra, 
present after a few hours, very rare exceptions excluded, a, some- 
times most accentuated, reaction of hypersensibility. Such a reac- 
tion manifest itself by dullness, drowsiness, and a state of semicoma, 


or by a strong physical and nervous excitability. Such phenomena 
are accompanied in either case by a remarkable acceleration of the 
pulse, dyspnoea, rising of temperature so far as 40° C, and often 
also vomit and increase in peristaltic movements, with excretion of 
diarrhoic dregs, mixed with blood and, sometimes, acutization of 
cutaneous preexisting eruptions. 

2. The difference in the reaction, due to such inoculation, upon the 
pellagra patients and upon the sound ones, is so remarkable that there 
is not appreciable reaction in the latter, in most cases, even if treated 
with doses eight or ten times stronger than those which are sufficient 
to provoke an evident reaction with the former. 

3. The hypersensibility, which manifests itself in pellagra pa- 
tients, owing to the inoculation of this watery extract of spoiled 
maize, has particular characters, which can not be found in any pro- 
portion through the injection of extract of sound maize. 

4. The active substance, which determines such a reaction of the 
watery extract of spoiled maize, is obtained by adding a given volume 
of the grain (deteriorated by mycotic action and not rotten), after 
having been finely triturated, to three or four volumes of physio- 
logical solution of chloride of sodium ; by keeping the whole in infu- 
sion for six hours in a bagno-marie at 55° C. ; by philtering the liquid 
and by treating it, at last, with twenty times its volume of absolute 
alcohol. In such a way a precipitation of the active substance is 
obtained, in white flakes. 

5. The thus obtained active substance, to which we have given 
the name of " pellagrogenina," is soluble in water and not in alcohol ; 
it does not lose its activity at a temperature of 110°-115° C. ; it has 
only a slight degree of poisoning, both for the trial animals and for 
a sound man ; it is, on the contrary, decidedly poisoning for a pellagra 

6. The characters of reaction of hypersensibility in the pellagra 
patient, which evidently result when the watery raw extract of 
spoiled maize is injected into his body, are more notable, and par- 
ticularly when the pure pellagrogenina, dissolved in fit quantities of 
water, is employed. This pure material, when injected into non- 
pellagra patients, has given no appreciable reaction, in the most ex- 
perimented cases (90%). 

7. The results obtained in more than 100 experiments, which were 
made with this substance, cause us to consider it of a particular 
efficiency in the pathogenesis of pellagra, and, in the meanwhile, 
induce us to propose same as a practical means of anaphylactic reac- 
tion for the diagnosis of pellagra. 

In order to obtain, to such a purpose, the particular reaction in an 
appreciable degree, and not dangerous, for the persons suspected to be 
afflicted with pellagra, the first injection is to be limited to 1 ccm. of 


watery solution, sterilized at 100° C, of pure pellagrogenina, at 11 
per cent. 

If no positive result is obtained by a first injection, this may be 
experimented with a double dose. 


Prof. Gay, California : Prof. Pagliani states in reply to a question 
that the reaction differs from the tuberculin reaction in that it fails 
to give a purely local (V. Pirquet) skin reaction in the pellagrin. 

A. D. Hirschfelder : I have been much interested in the observa- 
tions of Prof. Volpino, for two years ago, in the Peoria Insane 
Asylum, I attacked the same problem by a slightly different method, 
as it was impossible, for various reasons, to try subcutaneous in- 
jections, as I had hoped to do. I tried the cutaneous reaction with 
extracts of good corn and spoiled corn by the same technique as 
the v. Pirquet skin puncture of skin. The punctures were made in 
the skin of the pellagrous area and the corn extract rubbed into the 
abraded area. Extracts of corn made with 10 per cent NaCe and 
0.2NaOH, alcohol, and ether were made. In all 13 cases of out- 
spoken pellagra and in 7 cases of individuals who had recovered 
from pellagra the year before the results were negative. These 
observations were published in the Archives of Internal Medicine, 
November, 1900. 

M. Moyell: Prof. Pagliani said in conversation that the diagnostic 
reaction resembles closely the general reaction to tuberculin injection 
as used for diagnostic purposes. This extract is injected in mini- 
mum dose and is followed soon after by temperature rises, et cetera, a 
general reaction which he considers specific as a diagnostic test. 

Prof. Pagliani points out that the injection of this extract causes 
an augmentation of symptoms. This augmentation, however, passes 
in a couple of days, and so, when the minimum dose is used, no 
serious consequences are involved. This diagnotic test is brilliantly 
successful for the purpose of resolving suspicious diagnosis in 


Von Dr. S. von Unterberger, St. Petersburg. 

Die Schilderung des Krankheitsbildes des Typhus grtinden wir 
dem heutigen Stande der Wissenschaft entsprechend auf das iitio- 
logische Prinzip. Yor etwa 50 Jahren wurde der Sammelbegriff 
Typhus in drei verschiedene Krankheiten geteilt: den Abdominal-, 
den Fleck- und Ruckfallstyphus. Im Jahre 1896 batten Achard 
und Bensaude den Paratyphusbazillus entdeckt und das Krank- 
heitsbild des Abdominaltyphus hatte als Erreger, ausser dem Eberth- 
Gaffkyschen Bazillus, noch andere erhalten, den Paratyphus A und 
B. Die grosse Bedeutung kommt dem zweiten Erreger zu. 

Dass ein Typhus durch verschiedene Erreger erzeugt werden kann, 
darf uns nicht besonders wundern; wird doch das Bild des Diabetes, 
Gelenkrheumatismus, Arteriosklerose etc. durch verschiedene auslo- 
sende Momente erzeugt. 

Die Gruppe Paratyphus lasst sich in zwei Unterabteilungen tren- 
nen und zwar in die Paratyphus B Gruppe und in die Gruppe Bac. 
enteritidis Gartner. Zur ersten gehoren der Schweinepestbazillus, 
Erreger der Kalberruhr, der Mausetyphusbazillns (Loffler), Erreger 
der Pseudotuberkulose bei Meerschweinchen, Erreger der infektiosen 
Enteritis des Papageien u. s. w. Zur zweiten Gruppe gehoren : Bazillen 
vom Typus Gartner, gefunden bei Fleischvergiftungen und hiernach 
beim Menschen, Erreger von infektioser Rattenenteritis etc. Die 
beiden Gruppen lassen sich durch spez. Immunitatsreaktionen tren- 
nen (Agglutination, Bakteriolyse, aktive Immunisierung, Komple- 
mentbildung) . 

Der Gartner'sche Bazillus erweist sich vor allem als Erreger der 
sog. Fleischvergiftung, aber auch bei gastrischen Erscheinungen 
bis zum Bilde der Cholera ist er gefunden. Makroskopisch lassen 
sich keine auffallig wahrnehmbaren Yeranderungen im Fleisch 
erkennen. Eine viel seltenere Form der Fleischvergiftung der 
Botulismus wird durch den B. botulinus erzeugt und ist auch klinisch 
vollig verschieden. 

Ausser Fleischvergiftungen erzeugen diese Bazillen auch Fischver- 
giftungen und Yergiftungen durch Mehlspeisen, Milchprodukte 
u. s. w. Mehl kann leicht durch kranke Mause infiziert, Massener- 
krankungen hervorrufen. Brod kann somit nicht selten ein Erreger 
der Epidemie werden. 

Die Eesistenz der Paratyphusbazillen gegen aussere Schadigungen 
ist im allgemeinen grosser, als diejenige der Eberth'schen Bazillen. 
Besonders erliegt er der Austrocknung nicht so schnell als dieser. 
Im Wasser bleibt er namentlich im Schlamm, unter Umstanden 
langere Zeit entwicklungsfahig. Durch Temperatur von etwa 70° 
wurde er erst nach ungefahr 10 Minuten getotet, was sehr wichtig 
ist, denn hohere Temp, wie 70° C. werden namlich im Innern 


grosserer Fleischstficke beim Kochen und Braten meist nicht erreicht. 
Gegen Desinfektionsmittel ist er im allgemeinen etwas resistenter als 
der Typhusbazillus. 

Der Para typhusbazillus ist im Gegensatz zu dem Typhusbazillus 
fiir verschiedene Tierarten ausserordentlich pathogen, namentlich 
fur Meerschweinchen und Mause. 

Die Paratyphus-Baz.-Infektion der Menschen verlauft meist unter 
dem Bilcle eines Abdominal typhus und vielfach ist es unmoglich 
allein auf Grund der klinischen Erscheinungen beide Krankheits- 
formen von einander abzugrenzen. Fiir Paratyphus sprechen: 
plozliches Erbrechen, Schiittelfrost, Herpes, harter Milztumor, 
Durchfall mit fakulentem Geruch, flohstichartige Roseola und 
leichter Verlauf. Bei der Sektion findet man die Darmschleimhaut 
stark geschwellt, haufig hamorrhagische F ollikelsch well im gen und 
Exulzerationen im ganzen Darm, Peyersche Driisen werden nur 
leicht geschwellt gefunden. Auch beim Paratyphus finden sich die 
Erreger in der ersten Krankheitswoche in nahezu 100 Prozent der 
Falle im Blute (Gallenanreichung) wie beim Abdominaltyphus. 

Die Verbreitungsweise des Paratyphus deckt sich mit der des Ab- 
dominaltyphus. Im Vordergrunde stent die Kontakinfektion, ebenso 
sind Trinkwasserepidemien beobachtet. In den letzten Jahren tre- 
ten besonders paratyphose Nahrungs : namentlich Fleischvergiftun- 
gen in den Vordergrund, was auf einen Zusammenhang der P.-T.- 
Infektion des Menschen mit gewissen Erkrankungen des Schlacht- 
viehes hinweist. Viele Bazillen der P.-Gartner-Gruppe gelangen 
auf dem Blutwege in die Organe und in das Fleisch der erkrankten 
Tiere, wo sie sich nach der Schlachtung vermehren und Gif tstoff aus- 
scheiden. Makroskopisch lassen sich keine auffallig wahrnehm- 
baren Veranderungen erkennen. Einwandfreies Fleisch kann nach- 
traglich infiziert werden von kranken Schlachttieren, wenn es zusam- 
men mit kranken aufbewahrt wird und mit infiziertem Wasser und 
Handen in Beriihrung kommt, weiter durch Mause und Ratten; 
Fliegen spielen wohl kaum eine Rolle bei der Entstehung von Epi- 

Auf Grund ailes Angefiihrten kommen wir zu f olgenden Schliissen : 

Der Typhus abdominalis (Eberth-Gaffky) und der Paratyphus 
(Schottmiiller) sind in klinischer, pathologisch-anatomischer und 
bakteriologischer Hinsicht wohl zu trennen und weisen viele Unter- 
schiede auf. Im Grossen und Ganzen ist aber das klinische Bild 
beider typhbsen Krankheiten dasselbe. In pathologisch-anato- 
mischer Beziehung sind bei Paratyphus B. ausser hamorrhagischen 
Erscheinungen vor allem ein Ergriffensein des ganzen Follikelap- 
parates des Darmes und geringe Infiltration die Peyerschen Driisen 
zu verzcichnen. In bakteriologischer Hinsicht ist der Erreger des 
P. Bazillus biologisch ein ganz anderer, gehort aber auch zur grossen 
Gruppe der Kolibazillen. 


Das alte pathologisch-anatomische Bild des Unterleibstyphus weist 
ja verschiedene Typen auf : entweder nur exulzerierende Peyersche 
Driisen odor neben leichter Infiltration derselben weit verbreitete 
Follikelinfiltration oder Exulzerationen oder beide Formen zusani- 
men von leichtem und schwerem Grade. Das klinische Bild ist 
dabei bald sehr schwer, bald mittelschwer, bald sieht man die Krank- 
heit auf den Fiissen durchmachen? Wie lassen sich diese Bilder 
erklaren? Wir miissen annehmen, dass in der Mehrzahl aller Ab- 
dominaltyphus-Epidemien aucli in friiheren Jahren stets mitverlief 
eine Paratyphus-Erkrankung. Die Bazillen der Paratyphusgruppe 
sind also mit dem Baz